Along similar lines, PGE2 secretion by BRAF-mutant melanoma cells considerably reduces the viability of mouse NK cells recruited to the TME, as well as their capacity to secrete CCL5 and X-C motif chemokine ligand 1 (XCL1) [132], which is critical for the recruitment of cross-presenting dendritic cells (DCs) and hence for the initiation of tumor-targeting adaptive immune responses that can be therapeutically actioned with ICIs [133]. The gene discussed is CCL5; the disease is melanoma.