Similarly, TGFβ1 has been suggested to polarize tumor-associated neutrophils (TAN) from an N1- to an N2-like phenotype, as the blockade of TGFβ1 in several murine tumor models enhances cytotoxic activity and proinflammatory cytokine production by tumor-infiltrating neutrophils, whereas the depletion of neutrophils in the context of TGFβ1-expressing tumors diminishes tumor outgrowth and is associated with enhanced intratumoral CD8+ T cell activation [94]. This evidence concerns the gene CD8A and neoplasm.