miR-34a, a well-established downstream effector of the tumor suppressor p53, contributes to the regulation of apoptosis and cell cycle arrest in CRC models [57,58]; miR-195-5p upregulation inhibits CRC proliferation via the downregulation of CDK2/CDK8 and the anti-apoptotic protein BCL2L2 [59] or by repressing FGF2 and Wnt/β-catenin signaling to inhibit tumor growth [60,61]. Here, BCL2L2 is linked to neoplasm.