Since mitochondrial dysfunction is a key player in the switch from simple steatosis to NASH and fibrosis, we deepened the role of PNPLA3, MBOAT7, and TM6SF2 “loss-of-function” mutations in mitochondrial dynamics by silencing MBOAT7 (MBOAT7−/−) and/or TM6SF2 (TM6SF2−/−, MBOAT7−/−TM6SF2−/−) in HepG2 cells carrying the PNPLA3 variant through CRISPR/Cas9 gene editing technology [6]. Here, MBOAT7 is linked to metabolic dysfunction-associated steatohepatitis.