Disruption of Crtam-Cadm1 contact in either Crtam or Cadm1 total KO mice led to a reduction of the CD4+CD8+ T cell population, and total loss of Crtam expression protected mice from induction of diabetes, thereby underlining the potential relevance of this interaction in mediating autoimmune destruction of pancreatic β cells (34, 35). The gene discussed is CD4; the disease is diabetes mellitus.