The treatment with ADA led to several biochemical events: (1) a significant suppression of proliferation in human melanoma cell lines through the induction of apoptosis; (2) a reduction in the nuclear translocation and activation of NF-κB; (3) decreased expression of anti-apoptotic proteins, including c-FLIP, XIAP, and Bcl-2; (4) inhibition of phosphorylation; (5) dysregulation of AKT protein and ERK activity; and (6) a substantial and dose-dependent reduction in the formation of lung metastatic foci in C57BL/6 mice. The gene discussed is AKT1; the disease is melanoma.