Moreover, Klemm et al. [223] suggested that inhibiting the neuroinflammatory signaling pathway CSF2Rβ-STAT5, which promotes tumor recovery, using the drug AC4-130 could sustain tumor control and classical microglial activation when another CSF1R inhibitor, BLZ945, is used to intervene in tumor-associated microglia/macrophages (Fig. 4C). The gene discussed is CSF1R; the disease is neoplasm.