Interestingly, provided that mutations in ALDH1a1 have been linked to alcoholism in humans (Liu et al., 2011), deletion of ALDH1a1 in mice not only attenuates GABA co-release but also causes behavioral effects including increased EtOH consumption and preference of EtOH over daily water in mice, implying that diminished GABA co-release due to an insufficient GABA supply is linked to alcoholism. The gene discussed is ALDH1A1; the disease is alcohol drinking.