F. nucleatum infection upregulated the expression of CPT1B, the rate‐limiting enzyme of FAO in CCSCs, and increasing evidence has shown that FAO is important for maintaining stemness and proliferation of CSCs, such as breast cancer stem‐like cells and quiescent leukemia progenitor cells.[4, 14] Thus, we hypothesized that F. nucleatum infection might enhance FAO rate in CCSCs, which in turn would promote proliferation and self‐renewal of CCSCs. The gene discussed is CPT1B; the disease is breast carcinoma.