INS and diabetes mellitus: 6‐OHDA selectively targets NE neurons by disrupting the amine uptake mechanism at sympathetic nerve terminals, while sparing dopaminergic (DA).[18, 19] As a result, NE release from sympathetic nerve endings is impaired, leading to reduced sympathetic drive to downstream targets.[20] In the NOD mouse model, 6‐OHDA treatment significantly increased diabetes incidence and mortality, accompanied by reduced serum insulin levels (Figure 2B–D).