Three proposals were offered to support the postulate: (1) there are shared genetic susceptibilities to both mycobacterial infection and T1D, (2) MAP is the source of the HSP65 protein, providing epitope homologies between mycobacterial HSP65 and pancreatic glutamic acid decarboxylase (GAD) and (3) epidemiologic findings tie the risk of T1D to early life exposure to cow’s milk (Dow 2006). The gene discussed is GAD1; the disease is type 1 diabetes mellitus.