In addition to these novel findings, we also observed previously reported high-impact mutations, including stop-gain mutations in LPL (rs328, chr 8-19962213-C-G) and LDLR (rs769737896, chr 19-11110759-C-T and rs769737896, chr 19-11110759-T-T) and splice donor site mutations in SLCO1B1 (rs571639279, chr 12-21141659-G-A) and CETP (rs2142001776, chr 16-56975153-T-C), further emphasizing the genetic heterogeneity of FH. The gene discussed is SLCO1B1; the disease is familial hyperaldosteronism.