Previously, we showed that blockade of the PH domain of PDK1 using a small cell-penetrating peptide suppressed phosphorylation levels of PDK1 and Akt, which resulted in a significant reduction in the viability and tube-forming ability of human umbilical vein endothelial cells (HUVECs), as well as a noticeable decrease in both pathological retinal angiogenesis and tumor vessel formation (Park et al., 2015). Here, PDK1 is linked to neoplasm.