NR3C1 and asthma: Unlike GR-α, GR-α does not bind to GC and acts as a weak dominant inhibitor of GR-α.32,34 Reduced GR-binding affinity, GR-overexpression, decreased histone deacetylase (HDAC) activity, and genetic predisposition all contribute to GC resistance asthma.35-37 The reduction in GR binding affinity has been linked to the expression of IL-4 and IL-2.38