In view of these results and currently available data, we postulate that stabilization of CCAT1/2 by m6A has an amplifying effect on MYC expression levels in cancer cells via 2 separate mechanisms: (i) Directly, through both lncRNAs acting as super-enhancers that positively regulate MYC mRNA [21]; (ii) Indirectly, by means of CCAT1/2 acting as microRNA sponges for MYC-targeting microRNAs let-7A and miR-145, respectively [50,51,52,53] (Figure 8). The gene discussed is MYC; the disease is cancer.