In summary, based on gene expression profile analysis results, we can speculate that different molecular mechanisms may contribute to the anticancer effect of D6 in melanoma cells: i) the induction of a cell stress response that triggers the ER stress-mediated apoptosis pathway; ii) the up-regulation of p53 signalling, which promotes p21- and GADD45-dependent cell cycle arrest as well as mitochondrial apoptosis based on Noxa over-expression; iii) the down-modulation of several growth signals, like both PI3K and NF-kB pathways, and c-kit receptor. The gene discussed is CDKN1A; the disease is melanoma.