LDLR and familial hyperaldosteronism: A pulse-chase study comparing unaffected and class II FH fibroblasts (the same mutation found in our FH iPSC) showed that the LDLR of normal fibroblasts had been transported to the Golgi for processing to the mature 160-kDa proteins, while 95% of the class II LDLR remained in the 120-kDa form (Yamamoto et al., 1980).