While SUV39H1 knockout impairs T cell effector response during infection, Niborski further found that in tumor models of B16F10-OVA and MCA-101 fibrosarcoma, SUV39H1-deficient mice demonstrated stronger antitumor activity in tumor-infiltrating lymphocytes (TILs) when combined with PD-1 ICB, compared to wild-type controls. Here, SUV39H1 is linked to neoplasm.