Moreover, because the phosphorylation of Ephexin1 at Ser16/18 by Akt, which is required for binding to K-Ras, is the key behind its tumor-promoting effects, it is reasonable to speculate that suppression of Ephexin1 phosphorylation will eliminate the tumorigenic effect in Ras-driven cancers. The gene discussed is AKT1; the disease is cancer.