Hendriks et al. developed a scalable, personalized hiPSC-organoid platform for investigating the etiology of steatosis (e.g., exogenous (overload nutritional diet) and genetic origins (PNPLA3 I148M high-risk variant and monogenic predisposition to lipid disorders)), for use with a drug-CRISPR toolkit for NAFLD target identification and testing [132,138,139]. This evidence concerns the gene PNPLA3 and metabolic dysfunction-associated steatotic liver disease.