Most importantly, knocking down of Drp1 with siDNM1L genetic intervention ameliorated the reduction in CPT1A and the abnormal LDs accumulation in HBx and AFB1 co‐exposed differentiated HepaRG cells, further highlighting that the shift of the mitochondrial dynamics toward fission mediated by Drp1 was involved in HBx and AFB1 co‐exposure‐triggered hepatic steatosis. The gene discussed is DNM1L; the disease is fatty liver disease.