By TEM we have shown that in conjunction with reduction of LD-ER contact sites there was an increase in LD-associated mitochondria with TOMM40 KD, an effect that may lead to increased trafficking of triglyceride-derived fatty acids via LDs into the mitochondria [65] as well as the upregulation of fatty acid oxidation that has been associated with MASLD [66]. The gene discussed is TOMM40; the disease is metabolic dysfunction-associated steatotic liver disease.