Although the exact mechanisms underlying HPA responsivity to stress are unknown (and likely complex), it has been demonstrated that there are individual differences in responsivity that are partially determined by genetic variants (e.g., FKBP5, CRHR1, NR3C1, NR3C2) that modify the effect of acute and chronic stress/trauma on cortisol levels in healthy adolescents and adults (Hartling et al., 2019; Starr et al., 2019; Utge et al., 2018) and patients with psychosis (Mondelli and Ciufolini, 2017). This evidence concerns the gene CRHR1 and psychotic disorder.