For instance, reversing the polarization of TAMs through CSF‐1R inhibition increased the short‐term survival.28 However, this strategy does not yield an increased long‐term survival because TAMs induce resistance to CSF‐1R inhibition through secretion of IGF‐1 and subsequent activation of PI3K signaling in tumor cells.29 This has spurred interest in finding novel and specific targets, with the goal of realizing the full potential of immune checkpoint blockade. The gene discussed is CSF1R; the disease is neoplasm.