Furthermore, the translocation to the plasma membrane of 78-kDa glucose-regulated protein GRP78, which facilitates M2 macrophage polarization of TAMs and tumor growth in lung cancer, was induced by IGF-1R signaling, and concomitant IGF-1 blockade and GRP78 knockdown in TAMs suppressed M2 macrophage-induced maintenance, proliferation, and migration of lung cancer cells (27). This evidence concerns the gene IGF1R and lung cancer.