P65 directly bind to the chemokine (CC‐motif) ligand 2 (CCL2) promoter, thereby increasing the CCL2 transcription and secretion in CAFs; CCL2, which was transcriptional activated by P65 in PDPN(+) CAFs, sustains tumor angiogenesis by interacting with ACKR1 and activating PI3K/AKT signaling in endothelial cells. This evidence concerns the gene AKT1 and neoplasm.