In breast cancer, prior studies have demonstrated that STAT3 directly binds to the promoter of CPT1B, promoting its transcriptional regulation, resulting in an enhanced FAO.[14] Consistently, we have demonstrated that STAT3 binds to the promoters of both CPT1A and CPT1B, and depletion of STAT3 leads to a decrease in the expression levels of CPT1A and CPT1B (Figure S4C–E, Supporting Information). This evidence concerns the gene CPT1B and breast carcinoma.