This is due, at least in part, to an exaggerated atopic response to the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), including upregulation of the keratinocyte stress-associated antigen Rae-1, which binds natural killer group 2D (NKG2D) on immune cells. The gene discussed is KLRK1; the disease is neoplasm.