Moreover, aberrant activation of STAT3 in myeloid cells promotes lung cancer by facilitating the recruitment of immunosuppressive cell types (e.g., regulatory T-cells (Tregs), MDSCs, alternatively activated macrophages) into the tumor microenvironment, while myeloid-specific deletion of STAT3 in mice unleashes anti-tumor immunity by enhancing cytotoxic T- and NK cell responses [48]. This evidence concerns the gene STAT3 and lung cancer.