In a CRISPR‐Cas9 screen of 35 human fetal hepatocyte organoids, FADS2 was identified as a key determinant of hepatic steatosis.[36] Interestingly, comparison of PNPLA3 knock‐out organoids with isogenic knock‐in PNPLA3 p.I148M and wildtype organoids showed that both knockouts and knock‐ins exhibited increased steatosis in contrast to the murine knockout model that does not induce steatosis.[142] These data reinforce the need for human cell models for studies of genetic predisposition in metabolic disorders. The gene discussed is FADS2; the disease is steatosis.