The entire list of functions of UCP2 and UCP3 is not known.[13] However, studies indicate that these proteins are involved in a negative-feedback loop limiting the concentration of reactive oxygen species (ROS).[14] Current scientific consensus states that UCP2 and UCP3 perform proton transportation only when activation species are present.[15] Among these activators are fatty acids, ROS, and certain ROS byproducts that are also reactive.[14][15] Therefore, higher levels of ROS directly and indirectly cause increased activity of UCP2 and UCP3.[14] This, in turn, increases proton leak from the mitochondria, lowering the proton-motive force across mitochondrial membranes, activating the electron transport chain.[13][14][15] Limiting the proton motive force through this process results in a negative feedback loop that limits ROS production.[14] Especially, UCP2 decreases the transmembrane potential of mitochondria, thus decreasing the production of ROS.