The authors attributed these results to a reserve of dopamine receptors at baseline (Nielsen and Andersen, 1992; Tadori et al., 2009; Covey et al., 2013), requiring either large-scale damage to dopaminergic structures (e.g., substantia nigra in Parkinson’s disease) or excessive receptor blockade (e.g., >80% D2R blockade for antipsychotic efficacy) for significant changes in blink rate. This evidence concerns the gene DRD2 and Parkinson disease.