CDKN2A and melanoma: When melanoma cell lines in vitro were treated with the same concentrations and intermittent schedule of decitabine that maintained or increased self-renewal of normal hematopoietic stem cells, decitabine induced cell cycle exit even in p16/CDKN2A and p53-null melanoma cells with morphologic changes of differentiation, up-regulation of the key melanocyte late-differentiation driver SOX9, restoration of the expected DCT/MITF ratio and up-regulation of canonical CDKN that mediate melanocyte cell cycle exit by differentiation [9].