Senescence facilitates stress-responsive cancer cells to adapt to altering environmental conditions primarily via epigenetic reprogramming.27 Our previous studies revealed that dacarbazine-induced melanoma cells exit from the cell cycle accompanied by transcriptional activation of focal adhesion signalling and enhanced adhesive capacities.24 Additionally, resting BRAF-positive melanoma cells treated with BRAF inhibitor exhibited similar phenotypic features. The gene discussed is BRAF; the disease is cancer.