RHO and atherosclerosis: SCAI is a negative regulator of Rho protein activation, particularly in the RhoA/DIAPH1 pathway.34 Prior studies indicate that DIAPH1 knockout in mice attenuates atherosclerosis progression, and downregulation of DIAPH1 expression has been observed in ischemic stroke patients.35–37 These findings suggest that SCAI may influence both structural and functional aspects of vascular biology, warranting further investigation as a potential target for atherosclerosis research.