In particular, Bcl-xL-induced regulation of chemokines could affect the ability of (i) CCL5 to drive NK cell infiltration in melanoma [58] or the response to immunotherapy [43, 59]; (ii) MCSF to induce a BRAF inhibitor resistant phenotype [60], or to promote fibroblasts activation or myeloid derived suppressor cells migration [61]; (iii) TNFα to contribute to melanoma invasion/growth and tolerance to MAPK inhibition [62, 63] and to MCSF secretion in macrophages [35], as well as to cooperate with IL-4 in protecting cancer cells from apoptosis [64]. This evidence concerns the gene BCL2L1 and melanoma.