Additionally, the TRAIL–TRAIL-R signaling in cancer cells has also been shown to facilitate the accumulation of a tumor-supportive immune environment by triggering an NF-κB-dependent gene activation, which elicited the production of cytokines, most importantly C‐C motif chemokine ligand 2 (CCL2), consequently promoting tumor growth via a CCL2/(C‐C motif) receptor 2 (CCR2) axis [147]. The gene discussed is CCL2; the disease is neoplasm.