Taken together, we demonstrate that the m6A reader IGF2BP3 induces LUAD p‐EMT with augmented cancer cell plasticity to facilitate metastasis through recognizing m6A‐modified MCM5 mRNAs depending on canonical m6A writers such as METTL3 to stabilize them, and that high‐level MCM5 proteins bind NICD1 to competitively abrogate SIRT1‐induced deacetylation and degradation of NICD1, leading to Notch signaling overactivation (Figure 7K). Here, IGF2BP3 is linked to cancer.