IGF2BP3 and pancreatic neoplasm: IGF2BP3, an m6A reader, binds to m6A‐modified transcripts, enhancing their stability, with c‐Myc being not only a classical target of IGF2BP3 but also a regulatory protein for various transporter proteins.[21] When pancreatic cancer cell‐derived EVs acted on PSCs, c‐Myc protein expression was upregulated, and this effect was more significant in GEM‐resistant pancreatic cancer cell‐derived EVs (Figure5A; Figure S6A, Supporting Information).