RAC1 and Adams-Oliver syndrome: For example, Adams-Oliver syndrome (AOS) patients have aplasia cutis and multiple additional congenital anomalies, and skin fibroblasts from AOS families with a mutation in a Cdc42/Rac1 regulatory protein (ARHGAP31) showed an enhanced cell migration rate and a reduced cell proliferation rate in vitro, as seen here in ACCBMS1(p.R930H) fibroblasts [3].