To test whether the Tlcd1/2 deletion-induced changes in the mitochondrial PE composition had an impact on liver disease development, we initially modeled NAFLD-associated lipotoxicity and inflammation in vitro by challenging cultured mouse primary hepatocytes with pro-inflammatory activators LPS endotoxin and the SFA palmitate (PA)29. The gene discussed is TLCD1; the disease is metabolic dysfunction-associated steatotic liver disease.