PCSK9 inhibitors, including monoclonal antibodies and siRNA therapies, prevent the degradation of LDLR on hepatocyte surfaces, showing remarkable efficacy in reducing LDL‐C and atherosclerotic events in patients with familial hypercholesterolemia.[22] Previous studies have shown that hepatocyte‐specific deletion of Srebf2 did not affect liver LDLR protein levels,[15] suggesting that PCSK9 inhibition might have additive effects on cholesterol reduction when combined with hepatic SREBP2 depletion. This evidence concerns the gene LDLR and familial hypercholesterolemia.