Our study also confirmed the upregulation trend of NFE2L3 in CRC patients, suggesting that inhibiting oxidative stress and inflammatory response may help alleviate the impact of NFE2L3 on CRC.TMCC3, previously characterized as a breast cancer stemness maintainer through AKT activation (29), has emerged as a potential RC progression driver, with our survival analysis linking its expression to adverse outcomes. This evidence concerns the gene AKT1 and breast carcinoma.