To investigate the mechanism underlying the tumor-suppressive role of myeloid-intrinsic PDLIM2 in lung cancer, we simultaneously deleted STAT3 or RelA from myeloid cells in PDLIM2mKO mice because STAT3 and RelA are 2 of the most well-known and best-studied targets of PDLIM2 (17–19, 29–31). Here, PDLIM2 is linked to neoplasm.