In addition, while the improved tumor control in Tipe2ΔNK/ΔNK mice was compromised by further deletion of Prf1 in Tipe2ΔNK/ΔNK; Prf1ΔNK/ΔNK mice, tumor growth in Tipe2ΔNK/ΔNK; Prf1ΔNK/ΔNK mice was similar to tumor growth in Prf1ΔNK/ΔNK mice (Figure 4E), suggesting that the improved tumor control by NK‐specific Tipe2 deletion requires perforin‐dependent NK cell antitumor effector functions. This evidence concerns the gene PRF1 and neoplasm.