Beyond genetic factors, other hypotheses were formulated, such as the presence of the Tau Disease Protein 43 (TDP-43) pathology [45], deriving from the accumulation of truncated/phosphorylated forms of the nuclear protein TPD-43, Vitamin B5 deficiency [46], Fyn kinase overexpression [47], cyclin dependent kinase 5 (Cdk5) hyperactivation [48], and many others. The gene discussed is CDK5; the disease is hyperinsulinemic hypoglycemia, familial, 4.