UCP2 and hereditary elliptocytosis: Significantly, chemogenetic inhibition of SNrGAD2 expressing GABA population (Gi) or targeted overexpression of mitochondrial uncoupling protein 2 (Ucp2 OE) in such population could ameliorate neuronal oxidative stress and mitochondrial dysfunction, and finally reverse HE-induced bradykinesia (green evidence chain on the right).