Likewise, we described the pivotal role played by Bcl-2 in orchestrating the crosstalk between melanoma cells and tumor microenvironment (TME) components, such as neovascular endothelial cells, through a mechanism involving vascular endothelial growth factor (VEGF), and tumor-associated macrophages through interleukin-1β induction of the M2 phenotype [11, 15, 16]. This evidence concerns the gene BCL2 and neoplasm.