It has been reported that overexpression of IL‐36γ in tumor cells in synergy with IL‐12 promotes type I immune responses to promote tumor regression and that IL‐36γ promotes IL‐17 production by γδTCR+ cells and CD4+ T cells in skin inflammation.[32, 44] However, knockout of IL‐36γ did not affect lymphocyte infiltration in tumor‐burdened lungs in the KL mouse model (Figure S4A, Supporting Information). Here, IL17A is linked to neoplasm.