Since EF-Tu displays chaperone activity in the quality control of misfolded newly synthesized polypeptides in mitochondria in a GTP-independent manner [23,24], we speculated that when EF-Tu was down-regulation, the peptides synthesized from mitochondria ribosomes may be misfolded, which may lead to tumor development and/or progression [25,26]. The gene discussed is EEF1A1; the disease is neoplasm.