Considering the limited information available on the biological mechanisms underlying the dynamic cellular plasticity between the EMT-like and MET-like states, CD36 could emerge as an active metabolic biomarker for therapeutic resistance, and in turn, its specific inhibition in HER2 + BC cells could promote a MET-like stemness phenotype, consequently increasing sensitivity to anti-HER2 drugs, as demonstrated by our preclinical data. The gene discussed is ERBB2; the disease is breast cancer.