The ASCVD risk in individuals with FH is proportionate to the cumulative LDL-C burden, and treatment options consist of lipid-lowering pharmacotherapies, including statins and non-statin therapies (e.g., ezetimibe, PCSK9 inhibitors, inclisiran, and evinacumab), as well as plasma apheresis [30,31,32]. The gene discussed is PCSK9; the disease is familial hyperaldosteronism.