These findings also substantiated earlier PET work with the same ligand showing that an increase in dlPFC D1R is associated with working memory impairment in schizophrenia (although not healthy volunteers), which was interpreted as a compensatory upregulation in response to chronic deficits in DA tone, but could also be a sign of excessive DA D1R signaling impairing working memory early in the disease process [188, 189]. This evidence concerns the gene DRD1 and schizophrenia.