We modeled a variety of different steatosis triggers and studied their interplay: (1) free fatty acid (FFA) loading to approximate a Western diet, (2) interindividual genetic risk through modeling the top risk variant, PNPLA3 I148M and (3) monogenic lipid disorders through creation of APOB or MTTP knockout (KO) organoids. The gene discussed is APOB; the disease is steatosis.