Regarding genetic models of PD, it has been shown recently that the bilateral SNc lesion (64% of loss considered as mild) in rats overexpressing human A53T mutated α-synuclein, enhanced waiting impulsivity (increases of the premature response rate using the 5-choice serial reaction time task) and that this behavior was further exacerbated with long-term administration of pramipexole in both OFF and ON states (Jiménez-Urbieta et al., 2019). The gene discussed is SNCA; the disease is Parkinson disease.