We recently reported a comparative metabolomic analysis of serum and tumor tissues before and after metformin treatment stratified by response as measured by decreased abundance of the proliferation antigen MKI67 in tumor tissues by immunohistochemistry (IHC) analyses.4 Metformin responders exhibited significantly decreased levels of phospho‐PRKAA2 as well as several downstream mTOR targets in tumor tissues, and the serum metabolome reflected activated lipolysis suggesting the activation of fatty acid metabolism following metformin treatment. Here, MTOR is linked to neoplasm.