The new OXIDs24 induced cell cycle arrest and inhibited AKT phosphorylation in non-small cell lung cancer cells (which overexpress the PI3K/AKT/mTOR pathway and show resistance to EGFR inhibitors), suggesting that the OXID nucleus can be used as central core to develop inhibitors of the PI3K/AKT/mTOR pathway. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.