Thus, the proliferation and clone formation ability of CRC cells increased, and cell apoptosis was inhibited both in vitro and in vivo. Hence, we found a novel regulatory mechanism underlying the m6A reader IMP2, which was placed in the IMP2–ZFAS1–OLA1 signaling axis for CRC tumorigenesis and progression. This evidence concerns the gene IGF2BP2 and colorectal carcinoma.