Although it is a matter of speculation, the autoreactive Th1/Th17-like cells detected in ACD-like lesions may be inhibited in vivo by immunosuppressive cells other than CD4+ T-cells as these lesions display a weak inflammation phenotype compared with AD-like lesions and no sign of autoimmune disease and may play a role of inhibiting the generation of autoreactive CD8+ T-cells in changing AD-like lesions into ACD-like lesions. The gene discussed is CD8A; the disease is granular corneal dystrophy type II.