In addition, the pathophysiology of pancreatogenic diabetes is multifactorial, with different potential contributions in a given patient resulting from (a) loss of mass of pancreatic islet cells, especially beta cells; (b) autoimmunity; (c) local and systemic inflammatory response; (d) mutations of the CFTR (CF transmembrane conductance regulator) proteins; (e) deficiency of fat-soluble vitamins A, D, E, and K; and (f) disruption of the insulin-incretin axis (nesidioblastosis) [47,48,49,50,51] (Figure 3 and Figure 4). This evidence concerns the gene INS and diabetes mellitus.