As expected, our findings showed that DNA damage-related proteins [24, 35, 36], including P-ATM, P-ATR, P-CHK2 and γH2AX as well as P53 and its downstream P21, were significantly increased after VB1 treatment (Fig. 4a), which suggests that VB1 inhibits melanoma cell growth through DNA damage that eventually leads to P53 pathway-related cell cycle arrest and apoptosis. The gene discussed is CDKN1A; the disease is melanoma.