In addition, in chemotherapy-resistant breast cancer cells, ERRγ, a subtype of estrogen receptor-associated receptors (ERRs), is upregulated due to the mRNA splicing of the precursor ESRRG triggered by N6-methyladenosine (m6A), and interactions between the high expression of ERRγ and p65 enhanced the transcription of CPT1B, which in turn facilitated FAO to mediate chemotherapy cancer cell resistance [93]. This evidence concerns the gene CPT1B and cancer.