In the present study we also showed that mitochondrial proteins, such as OPA1 and cytochrome C, that we previously reported down-regulated in models of cancer- or chemotherapy-induced muscle wasting [2,43], were reduced in cardiac muscle with MKI treatment, whereas these same proteins were unchanged in skeletal muscle, also in line with previously published evidence investigating the mitochondrial toxicity induced by sorafenib [31,47] or supporting the MKI-induced disruption of mitochondrial membrane polarization in tumor cell lines [48]. This evidence concerns the gene OPA1 and cancer.