To further elucidate the modulation of macrophage phenotypes for the purpose of anti-tumor therapy, particularly focusing on the conversion of M2 macrophages to the pro-inflammatory M1 phenotype, previous studies showed promise in reprogramming macrophages toward an anti-tumor state using Toll-Like Receptor agonists, such as MPLA (77), and CSF1R inhibitors, such as pexidartinib (78, 79). Here, CSF1R is linked to neoplasm.