Notably, the compound KO model runs into metabolic reprogramming towards anaerobic glycolysis, supporting that the co-absence of TM6SF2 and MBOAT7 deletions together with the presence of the PNPLA3 p.I148M mutation may synergically affect mitochondrial metabolism within the hepatocytes thus contributing to progressive liver damage and possibly triggers the switch towards HCC [248,249]. This evidence concerns the gene MBOAT7 and hepatocellular carcinoma.