Consistent with this, Lv et al. supported a GBM therapeutic role by targeting METTL3, which reported that upregulation of METTL3 expression by platelet-derived growth factor receptor (PDGFR) signaling promoted mitophagy regulator OPTN (optineurin) mRNA degradation to suppress tumor [58] (Table 1). The gene discussed is OPTN; the disease is glioblastoma.