In the presence of TIPE2, tumor growth was not affected significantly by conditional knockout of perforin in NK cells (Prf1ΔNK/ΔNK mice) (Figure 4E), possibly due to the minimal contribution to overall tumor control by perforin‐dependent antitumor effector functions of the exhausted tumor‐infiltrating NK cells, which was diminished by TIPE2. The gene discussed is TIPE2; the disease is neoplasm.