The loss of β-cell function in IDDM is mediated principally by CD4+ and CD8+ T cells, and autoreactive effector CD8+ T cells (CTLs) were shown to be responsible for islet β-cell destruction in the non-obese diabetic (NOD) mouse and in human IDDM (4–6). The gene discussed is CD4; the disease is type 1 diabetes mellitus.