These findings suggest that chronic inflammation and oxidative stress associated with metabolic disorders may amplify ERBB2-mediated oncogenic signaling, potentially through enhanced activation of PI3K/AKT/mTOR and MAPK/ERK pathways.25,26 The interplay between metabolic stress and ERBB2 overexpression may also promote an immunosuppressive tumor microenvironment, further exacerbating tumor progression.11,27,28. The gene discussed is MTOR; the disease is metabolic disease.