In this research, we clarified that overexpressed HMMR remarkably promoted mTOR phosphorylation at Ser2448 and AKT phosphorylation at Ser473 in a partially AURKA-dependent manner, which shed light on another pathway of mTORC2/AKT activation and further strengthened the theoretical basis for the application of mTOR inhibitors to control tumour progression. The gene discussed is HMMR; the disease is neoplasm.