Despite their clinical benefits, mTOR inhibitors, including rapamycin and its analogs (e.g., everolimus and temsirolimus), encounter challenges such as drug resistance, adverse effects, and limitations of efficacy.71,72 A known disadvantage of mTOR inhibitors is their tendency to activate AKT pathways via a feedback mechanism, which may favor tumor survival and undermine therapeutic outcomes.73 Similarly, EGFR inhibitors always end up with drug resistance.74 To overcome these barriers, combined administration of mTORC1 and EGFR inhibitors was tested in clinical trials. The gene discussed is AKT1; the disease is neoplasm.