Among these, CNK2, which is implicated in non-syndromic X-linked intellectual disability [97], was reported to form a multiprotein complex with cytohesin-2 and Rac/Cdc42 signaling molecules, such as Rac1 itself, Rac/Cdc42-GEFs (α-PIX and β-PIX), and Rac/Cdc42-GAP (Vilse/ARHGAP32), and to regulate dendritic spine morphogenesis in hippocampal neurons [51], suggesting that CNK2 may serve as a platform that connects Arf signaling to the Rac/Cdc42 pathway in the dendritic spine. Here, CNKSR2 is linked to X-linked intellectual disability.