The group of Musso et al. [3] showed convincing results, indicating that GIP response to saturated fatty acids (SFA) ingestion is prolonged in non-diabetic patients with NASH and is correlated with liver disease, an unfavorable dynamic adipokine profile, and β cell dysfunction, which provides a rationale for GIP antagonism in these subjects [3]. This evidence concerns the gene GIP and metabolic dysfunction-associated steatohepatitis.