HK2 and colorectal neoplasm: cd36 -GPC4相The CD36-GPC4 interaction promotes proteasome-dependent ubiquitination of GPC4, thereby inhibiting the β-catenin/c-myc signaling pathway and downstream glycolytic target genes GLUT1, HK2, PKM2, and LDHA. Furthermore, the knockout of CD36 significantly increased the occurrence of colorectal tumors in inflammation-induced CRC models and ApcMin/+ mouse models.