Interestingly, Huang et al. proposed the potential identification of hyper-methylated transcripts in ovarian cancer cells via IGF2BP1-3 as an RNA binding protein, which leads to increased transcript stability and gene expression levels [110] Overexpression of wild-type FTO was shown to otherwise inhibit ovarian cancer stemness and tumorigenesis, while mutant enzymatically-inactive forms failed to do so; highlighting the necessary role of FTO as m6A demethylase in ovarian cancer [109]. The gene discussed is FTO; the disease is ovarian cancer.