Indeed, treatment of CRC cells with Cud C induced significant reduction in AKT phosphorylation in 2 independent CRC cells (KM12 and Caco-2), while the ectopic expression of constitutively active myristoylated AKT completely abrogated the antitumor effects of Cud C. These results suggest that the antitumor effect of Cud C is PI3K-AKT dependent. Here, PIK3CD is linked to colorectal carcinoma.