Gene redundancy is the existence of multiple genes in the genome of an organism that perform the same function. Gene redundancy can result from gene duplication. Such duplication events are responsible for many sets of paralogous genes. When an individual gene in such a set is disrupted by mutation or targeted knockout, there can be little effect on phenotype as a result of gene redundancy, whereas the effect is large for the knockout of a gene with only one copy. Gene knockout is a method utilized in some studies aiming to characterize the maintenance and fitness effects functional overlap.

Classical models of maintenance propose that duplicated genes may be conserved to various extents in genomes due to their ability to compensate for deleterious loss of function mutations. These classical models do not take into account the potential impact of positive selection. Beyond these classical models, researchers continue to explore the mechanisms by which redundant genes are maintained and evolve. Gene redundancy has long been appreciated as a source of novel gene origination; that is, new genes may arise when selective pressure exists on the duplicate, while the original gene is maintained to perform the original function, as proposed by newer models.

Gene redundancy most often results from Gene duplication. Three of the more common mechanisms of gene duplication are retroposition, unequal crossing over, and non-homologous segmental duplication. Retroposition is when the mRNA transcript of a gene is reverse transcribed back into DNA and inserted into the genome at a different location. During unequal crossing over, homologous chromosomes exchange uneven portions of their DNA. This can lead to the transfer of one chromosome's gene to the other chromosome, leaving two of the same gene on one chromosome, and no copies of the gene on the other chromosome. Non-homologous duplications result from replication errors that shift the gene of interest into a new position. A tandem duplication then occurs, creating a chromosome with two copies of the same gene. Figure 1 provides a visualization of these three mechanisms. When a gene is duplicated within a genome, the two copies are initially functionally redundant. These redundant genes are considered paralogs as they accumulate changes over time, until they functionally diverge.

Much research is centered around the question of how redundant genes persist. Three models have arisen to attempt to explain preservation of redundant genes: adaptive radiation, divergence, and escape from adaptive conflict. Notably, retainment following a duplication event is influenced by type of duplication event and type of gene class. That is, some gene classes are better suited for redundancy following a small scale duplication or whole genome duplication event. Redundant genes are more likely to survive when they are involved in complex pathways and are the product of whole genome duplication or multifamily duplication.

The currently accepted outcomes for single gene duplicates include: gene loss (non-functionalization), functional divergence, and conservation for increased genetic robustness. Otherwise, multigene families may undergo concerted evolution, or birth and death evolution. Concerted evolution is the idea that genes in a group, such as a gene family, evolve in parallel. The birth death evolution concept is that the gene family undergoes strong purifying selection.

As the genome replicates over many generations, the redundant gene's function will most likely evolve due to Genetic drift. Genetic drift influences genetic redundancy by either eliminating variants or fixing variants in the population. In the event that genetic drift maintains the variants, the gene may accumulate mutations that change the overall function. However, many redundant genes may diverge but retain original function by mechanisms such as subfunctionalization, which preserves original gene function albeit by complementary action of the duplicates. The three mechanisms of functional divergence in genes are nonfunctionalization (or gene loss), neofunctionalization and subfunctionalization.

During nonfunctionalization, or degeneration/gene loss, one copy of the duplicated gene acquires mutations that render it inactive or silent. Non-functionalization is often the result of single gene duplications. At this time, the gene has no function and is called a pseudogene. Pseudogenes can be lost over time due to genetic mutations. Neofunctionalization occurs when one copy of the gene accumulates mutations that give the gene a new, beneficial function that is different than the original function. Subfunctionalization occurs when both copies of the redundant gene acquire mutations. Each copy becomes only partially active; two of these partial copies then act as one normal copy of the original gene. Figure 2 to the right provides a visualization of this concept.

Transposable elements play various roles in functional differentiation. By enacting recombination, transposable elements can move redundant sequences in the genome. This change in sequence structure and location is a source of functional divergence. Transposable elements potentially impact gene expression, given that they contain a sizeable amount of micro-RNAs.