Furthermore, we also demonstrated that the BX795-mediated pharmacologic targeting of PDK1 resensitizes HCC cells to IR-induced apoptosis signals dose-dependently, and significantly suppress their oncogenicity (Figure 5), which is consistent with findings showing that PDK1 signaling is critical for the growth and survival of cancerous cells, and that small-molecule inhibition of PDK1/PLK1 activity effectively targeted and impaired MYC dependency with its associated therapy resistance [24]. The gene discussed is PLK1; the disease is hepatocellular carcinoma.