Furthermore, the Leptin‐JAK/STAT3 pathway upregulated the expression of CPT1B, FAO activity, and stem cell self‐renewal in breast cancer.[18b] In the context of HCC, the potential mechanisms by which FAO elevation maintains self‐renewal ability have been reported.[38] Our results indicated that HK2 could also be contributed to the effect of FAO activity on CSC stemness maintenance. This evidence concerns the gene CPT1B and breast carcinoma.