Based on such results, we can speculate that: a) p53 protein may play a key role in sustaining the anticancer effects exerted by D6 on melanoma cells; b) induction of strong cell stress responses may contribute to the reinforcement of the proapoptotic trend of p53 signalling; and c) down-modulation of several growth signals (c-kit, PI3K/Akt and NF-kB), as well as the under-expression of cell cycle regulators (cyclin B, cdc25 and CDK4) might be involved in cell growth inhibition. Here, AKT1 is linked to melanoma.