CCL2 and neoplasm: CDYL deficiency augmented the antitumor response and hindered tumor growth in vivo. It resulted in increased expression of chemokine ligands (CXCL12, CCL2), which contributed to monocyte and macrophage recruitment. CDYL knockdown elevated the influx of M1-like tumor-associated macrophages/microglia (TAMs), and decreased the population of M2-like TAMs.