Next, we found that by using antibodies to HNRNPA2B1 in PCa cell lysates, pri-miR-93 was enriched (Figure 4E), while depleting METTL3 inhibited this interaction (Figures 4F and S2D, E), suggesting that the m6A placement on pri-miR-93 by the m6A reader METTL3 was necessary for the recognition of HNRNPA2B1. The gene discussed is METTL3; the disease is posterior cortical atrophy.