To point out whether the oncogenic roles of patient derived PDK1 mutations due to elevating the AKT activity, we depleted AKT1 in either Type I or Type II mutant PDK1-expressing colon cancer cells (Supplementary Fig. 9a), and observed that knockdown AKT1 markedly compromised the oncogenic roles of mutant PDK1 in promoting colony formation (Supplementary Fig. 9b, c). This evidence concerns the gene PDK1 and malignant colon neoplasm.