Loss-of-function mutations in RAC1 and other genes of the Rac signaling pathway have been implicated in the pathogenesis of Intellectual Disability (ID).
Such insights may have implications for the utility of Rac1 inhibitors in the treatment of intellectual disability caused by <i>Cc2d1a</i> mutations in human patients.
Misregulated RhoA, Rac1/Rac3 and cdc42 activity has been linked with intellectual disability (ID) and other neurodevelopmental conditions that comprise ID.