However, particularly in those with FH and previous ASCVD or in those with high subclinical atherosclerosis burden, there is the unmet need of still-elevated LDL-C [14,38], and these patients will often require a third-line pharmacological intervention such as PCSK9 inhibitors to achieve the target LDL-C goals [55,56]. The gene discussed is PCSK9; the disease is familial hyperaldosteronism.