A novel inhibitor of AKT1–PDPK1 interaction is reported to efficiently restrict tumor growth in prostate cancer.32 Here we show that PDPK1 is significantly associated with RCC patient's survival after treatment, notably, we demonstrate that CYD-6-17 can target PDPK1 and its downstream AKT, subsequently, effectively inhibits RCC cell growth, thus discover a novel anticancer target and provided a promising therapeutic strategy. Here, AKT1 is linked to neoplasm.