Furthermore, it has been reported that a stronger relationship between the m6A reader YTHDF3 and DICER1-AS1 leads to DICER1-AS1 degeneration as a consequence of glucose exhaustion, and YTHDF3 has an essential focus of miR-5586-5p through which it can form a negative feedback loop with DICER1-AS1 to promote the process of glycolysis in pancreatic cancer (Hu et al., 2022). This evidence concerns the gene YTHDF3 and pancreatic neoplasm.