In a different context, the lung intratumoral bacterial load promotes the expansion and accumulation of a distinct RORγt+, IL-17A+ γδ T cell population in the lung TME of a mouse model of human LUAD, which further produces tumor cell proliferation mediators, such as IL-22, that drive neutrophil infiltration and potentiate tumor growth [155]. This evidence concerns the gene IL17A and neoplasm.