The group of Schnackenberg et al. has shown that chronic inhibition of HSD11B1 activity, meaning inhibiting the back-conversion of cortisone to cortisol, decreases hypertension, insulin resistance, and hypertriglyceridemia in metabolic syndrome [49], which points out that cortisol is a negative trigger in some conditions, especially in MR expressing tissues lacking HSD11B2. This evidence concerns the gene HSD11B2 and metabolic syndrome.