This acetylation‐related stabilization of METTL3 by ACAT1 suppresses TNBC cell migration and invasion, highlighting how the NR2F6/ACAT1/METTL3 axis plays a crucial role in reducing tumor aggressiveness.[113] In addition, acetylation controls METTL3 localization and function, with nuclear METTL3 promoting breast cancer metastasis through an IL‐6‐dependent mechanism that enhances m6A methylation. This evidence concerns the gene ACAT1 and breast carcinoma.