Recent conceptualizations reconcile these seemingly disparate findings (i.e., KOR activation implicated in both increased and decreased drinking) by proposing that EtOH upregulates expression of dynorphin, an endogenous KOR ligand (Chavkin, James, & Goldstein, 1982) often associated with states of stress and dysphoria (see Bruchas, Land, & Chavkin, 2010; Van't Veer & Carlezon, 2013). The gene discussed is OPRK1; the disease is dysphoria.