Additionally, with the alterations in cecum and gut observed in Nile rats [1] and the functional role of intestinal K-cells and L-cells in mind, cellular damage or a decrease in the secretion of GIP, GLP-1, and PYY might contribute to the consumption of extra calories by Nile rats or a human population that preferentially selects highly-processed foods and, in turn, influences T2DM risk [87]. The gene discussed is GIP; the disease is type 2 diabetes mellitus.