Some chemotherapeutics such as taxol, vincristine or etoposide modify non‐metabolic targets like the cytoskeleton or affect DNA replication.[21, 22] The PI3K/AKT/mTOR signaling pathway is another prominent target for cancer treatment since it controls the metabolic activity of key CCEM pathways.[23, 24] Since these targets may, therefore, have indirect effects on the CCEM, it is crucial to investigate whether metabolic patterns derived from cell treatments with microtubule inhibitors, topoisomerase inhibitors, or PI3K/AKT/mTOR inhibitors accurately predict their MoAs. The gene discussed is MTOR; the disease is cancer.