Recently, using a T1D mouse model induced by CD8‐OTI cells, it was shown that the interaction of CRTAM with its ligand, nectin‐like‐2 (Necl‐2), was necessary for CD8+ auto‐reactive lymphocyte retention in pancreatic lymph nodes and their further activation, proliferation, and differentiation into an optimal effector phenotype 12. The gene discussed is CRTAM; the disease is type 1 diabetes mellitus.