The original neural diathesis-stress model of schizophrenia (Walker and Diforio, 1997) and subsequent revisions of this hypothesis (Pruessner et al., 2017; Walker et al., 2008) hypothesized that heightened HPA axis activity among those at elevated risk for psychosis could be stress-induced, a manifestation of hippocampal dysfunction or glucocorticoid receptor abnormalities, or genetically determined. This evidence concerns the gene NR3C1 and psychotic disorder.