ARHGEF2 and colorectal carcinoma: Emerging evidence highlights the critical role of m6A modifications in colorectal tumorigenesis.12–14 For instance, METTL3 has been demonstrated to facilitate CRC through activating mTOR signaling.12 YTHDF1 also accelerates CRC development by promoting ARHGEF2 translation and RhoA signaling.13 Whereas ALKBH5 upregulation in CRC cells recruits myeloid-derived suppressor cells (MDSCs) to suppress immune surveillance, leading to disease progression.14 These studies illustrate the multifaceted roles of m6A modification to CRC tumorigenesis.