In contrast, the SRGAP2B and SRGAP2D are highly copy number polymorphic, with normal individuals identified that completely lack these paralogscopies.

Incomplete duplication created a novel gene function—antagonizing parental SRGAP2 function immediately “at birth” 2–3 mya, which is a time corresponding to the transition from Australopithecus to Homo and the beginning of neocortex expansion.

SRGAP2C phenocopies SRGAP2 deficiency and underlies sustained radial migration and results in the emergence of human-specific features, including neoteny during spine maturation and increased density of longer spines.

It appears that the SRGAP2C ultimately assumed the antagonistic function of the SRGAP2B duplicate, which shows evidence of pseudogenization in contemporary humans.

It is unlikely that SRGAP2B and SRGAP2D are now functional as SRGAP2B has a markedly reduced expression in human brain compared to SRGAP2C and the transcripts produced by SRGAP2D lack two internal exons, leading to a premature termination codon.