IGF2BP3 and neoplasm: Several reports have also shown that Notch overactivation facilitates tumor cells to undergo p‐EMT and promotes tumor metastasis.[47, 48, 49] Although Notch signaling overactivation is commonly shown in metastatic tumor tissue, genetic alterations in genes involved in Notch signaling are rare in LUAD.[18, 19] In our present study, we demonstrate a m6A reader IGF2BP3‐mediated mechanism through which m6A‐dependent epigenetic overactivation of Notch signaling is achieved in LUAD cells undergoing p‐EMT.