A study showed that HMD led to significant activation of the ATF6/homocysteine-inducible endoplasmic reticulum protein (HERP) arm of ER stress in low-density lipoprotein receptor (LDLR)−/− mice, which induced phenotypic transformation of VSMCs; knockdown of HERP inhibited this process, attenuating HHcy-mediated atherosclerosis [75]. The gene discussed is LDLR; the disease is hereditary mucoepithelial dysplasia.