B2M and neoplasm: To support this conclusion, targeted deletion of B2m, an essential component of MHC-I, while having no effect on cell proliferation (Figure 1M and Supplemental Figure 2, A and B) as reported (16), totally abolished the increased CD8+ OT-I T cell-mediated killing of Usp22-deficient tumor cells (Figure 1N), as well as the activation and increased secretion of IFN-γ and TNF-α (Figure 1, O–Q, and Supplemental Figure 2, C–F).