Our study extends this relevance to radiation-induced T-ALL, showing that CD8+ T cells activated by LMP1/2A+B cells exhibit increased NKG2D expression, which enhances their ability to recognize and eliminate tumors lacking MHC class I. In future studies, we plan to use MHC class I-deficient tumor models or MHC class I–neutralizing antibodies to completely block the classical killing pathway, in order to further evaluate the roles of NKG2D, 2B4, and other potential mechanisms. The gene discussed is KLRK1; the disease is neoplasm.