Thus, in the present study, considering that cancer cells favor metabolism through glycolysis rather than efficient oxidative phosphorylation [25,26], the underlying oncogenic potential of MID1IP1 was explored in HCC growth in association with c-Myc signaling mediated by ribosomal protein L5 or L11 and CNOT2 in HCC cells and tissues. This evidence concerns the gene CNOT2 and hepatocellular carcinoma.