Although treatment with the inhibitory ASO vupanorsen targeting ANGPTL3 production was recently associated with dose-dependent increases in hepatic steatosis that led to its discontinuation (15, 16), humans with complete genetic deficiency of ANGPTL3 have reduced VLDL-ApoB100 production without an increase in prevalence or severity of hepatic steatosis (5, 17, 18). This evidence concerns the gene ANGPTL3 and fatty liver disease.