Studies from our group and others, aimed at establishing a mechanism for how PCSK9 inhibitors lower plasma Lp(a) levels, found that Lp(a) uptake by the LDLR in cultured human hepatoma cells can be modulated by PCSK9 [34, 37]; this provides a mechanistic basis for the ability of PCSK9 inhibitors to lower Lp(a) levels in humans. The gene discussed is PCSK9; the disease is hepatocellular carcinoma.