The entire list of functions of UCP2 and UCP3 is not known. However, studies indicate that these proteins are involved in a negative-feedback loop limiting the concentration of reactive oxygen species (ROS). Current scientific consensus states that UCP2 and UCP3 perform proton transportation only when activation species are present. Among these activators are fatty acids, ROS, and certain ROS byproducts that are also reactive. Therefore, higher levels of ROS directly and indirectly cause increased activity of UCP2 and UCP3. This, in turn, increases proton leak from the mitochondria, lowering the proton-motive force across mitochondrial membranes, activating the electron transport chain. Limiting the proton motive force through this process results in a negative feedback loop that limits ROS production.  Especially, UCP2 decreases the transmembrane potential of mitochondria, thus decreasing the production of ROS. Thus, cancer cells may increase the production of UCP2 in mitochondria. This theory is supported by independent studies which show increased ROS production in both UCP2 and UCP3 knockout mice.
This process is important to human health, as high-concentrations of ROS are believed to be involved in the development of degenerative diseases.