These systems emulate fatty acid‐induced steatosis and inflammation; moreover, evaluation of organoid stiffness can be used as a proxy for fibrosis.[63, 64, 65] Hepatic organoids can mimic the effect of genetic factors and CRISPR profiling of 35 genes has recently been used to identify FADS2 as an important determinant of hepatic steatosis.[66, 67] However, the use of organoids for MASH drug development is hampered by multiple factors. The gene discussed is FADS2; the disease is steatosis.