An additional mechanism of immune escape was demonstrated in human melanoma cells, in which BRAF V600E signaling impairs T cell-mediated antitumor responses by increasing the transcription of interleukin 1 alpha (IL-1a) and beta (IL-1b) in cancer-associated fibroblasts resulting in a reduction of their ability to kill melanoma cells [20]. The gene discussed is IL1A; the disease is melanoma.