While the mechanism of action of gold-containing drugs in most cancer types remains poorly understood, mechanistic studies in lung cancer cells demonstrate that ATM-mediated inhibition of transformed growth requires the gold-modifiable Cys69 residue in the PKCι PB1 domain, demonstrating the necessity for PKCι inhibition for the anti-tumor effects of ATM in lung cancer cells [4, 6, 19]. Here, PRKCI is linked to neoplasm.