Given that Hpa2-KO mice are not obese and seemingly do not exhibit metabolic syndrome(s), the fat accumulating in their pancreas is most likely due to the replacement of acinar cells by fat cells through acinar-to adipocyte-transdifferentiation (AAT) [24, 26], a form of epithelial-to-mesenchymal transition (EMT). The gene discussed is HPSE2; the disease is metabolic syndrome.