UQCRB and neoplasm: A number of authors have reported the effect of antioxidants, such as SkQR1, NAC, Mito-CP, and Mito-TEMPO [41,43,44] on the redox modulation of EMT; however, the involvement of the mitochondrial Complex III UQCRB site in the EMT reversion, due to the inhibition of the hypoxia-induced mitochondrial ROS production and the related decrease in HIF-1α stabilization, represents the novelty of this work and might provide a rationale for the development of drugs able to counteract tumor progression induced by the EMT by blocking mitochondrial ROS production at this site.