Indeed, increased mitochondrial import of proteins involved in ATP synthesis such as ATP5A and ATP5B, together with augmented citrate synthase, a key enzyme of TCA cycle, could mark a shift in tumor metabolism from glycolysis to oxidative phosphorylation pathway (OXPHOS) that could represent a mechanism of oxaliplatin resistance, such as has been unraveled in other tumor models [53]. The gene discussed is ATP5F1B; the disease is neoplasm.