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.
Loss-of-function mutations in RAC1 and other genes of the Rac signaling pathway have been implicated in the pathogenesis of Intellectual Disability (ID).
Misregulated RhoA, Rac1/Rac3 and cdc42 activity has been linked with intellectual disability (ID) and other neurodevelopmental conditions that comprise ID.