These studies suggest the anti-tumor activity of our NDRG1-inducing agents (16, 34, 37, 38, 39, 40, 41, 42, 98) and NDRG1 itself against multiple cancer-types (1, 2, 3, 4), could be mediated, at least in part, via its effect on PKCα expression. The gene discussed is PRKCA; the disease is neoplasm.