In addition to increasing LDL plasma levels, PCSK9 gain-of-function pathogenic variants have been found to increase circulating Lp(a) in FH patients (Tada et al., 2016), potentially by interfering with Lp(a) endocytosis, as shown in a human hepatocellular carcinoma model (Romagnuolo et al., 2015). The gene discussed is LPA; the disease is familial hyperaldosteronism.