Based on the results, it is appropriate to hypothesize that the de novo lipogenesis and exogenous FA uptake might be upregulated in HER2-positive breast cancer cells by PI3K/AKT/mTOR activation and, therefore, to evaluate therapeutics targeting PI3K in combination with SCD-1 or CD36 inhibitors in HER2-positive breast cancers. The gene discussed is MTOR; the disease is breast carcinoma.