It is one of the first Stat proteins identified in the IFN signal transduction pathways and has been implicated in suppressing tumor cell proliferation, differentiation, apoptosis, and angiogenesis.[43] A recent study has reported that Sta1 activation resulted in CCL2 stimulation, thereby provoking macrophage polarization.[44] Similarly, we found Stat1 could be elevated by IFN‐γ treatment in mouse RAW264.7 cells in vitro, and Stat1 transcriptionally upregulated CCL5 in macrophages. Here, STAT1 is linked to neoplasm.