These findings suggest that the MPE-Mφ with both M1 and M2 markers can be repolarized by IFN-γ and β-glucan through the activation of the JAK/STAT1 [32] and Syk-CARD9-ERK pathways [19] to downregulate the M2 markers TGF-β1 and CD163, thereby enhancing the repolarization of MPE-Mφ into tumor-inhibiting M1 macrophages (Fig. 5). This evidence concerns the gene STAT1 and neoplasm.