Intriguingly, Zhong et al.117 noticed that whole-body Cd36 deletion did not affect hepatic FFAs uptake in mice while increased monocyte chemotactic protein-1 transcription in hepatocytes and enhanced hepatic inflammation and fibrosis117, pointing out that Cd36 deficiency might contribute to NASH development by a fatty acid-independent mechanism. The gene discussed is CD36; the disease is metabolic dysfunction-associated steatohepatitis.