Most notably, m6A/MeRIP-seq and PARIS datasets allowed us to speculate that A5044 functions as an m6A switch, whereby m6A5044 stabilizes formation of PK7, which would occlude miRNA-binding sites, and unmethylated A5044 favors formation of PK7→HP, which would allow miR-101 and miR-217 to be sponged by MALAT1 in cancer (Figure 5) [27,42,43]. The gene discussed is MALAT1; the disease is cancer.