A greater capacity to internalize FAs, coupled with lower activity of the HER2-FASN axis, could lead to increased activity of the catabolic FA oxidation (FAO) pathway; increased FAO activity is associated with aggressive tumor features in BC [53], revealing a potentially new lipid metabolic vulnerability via the specific targeting of carnitine palmitoyl transferase 1 (CPT1A) with etomoxir/ST1326 inhibitors, which are already used clinically [54, 55]. This evidence concerns the gene FASN and breast cancer.