Interestingly, we found that GOLPH3 enhanced PDK1, mTOR, and AKT phosphorylation in the PDK1/mTOR/AKT signal pathway (data was not shown), which indicated crosstalk between the c-Myc/hTERT/cyclin D1 and PDK/mTOR/AKT signaling pathways, and could explain how the GOLPH3-STIP1 interaction induced tumor cell proliferation. The gene discussed is MYC; the disease is neoplasm.