Studies have demonstrated that oxidative stress not only perpetuates airway pathology but also impairs corticosteroid efficacy in asthma by reducing histone deacetylase 2 (HDAC2) activity, altering glucocorticoid receptor signaling, and activating pro-inflammatory pathways, all of which contribute to the emergence of steroid resistance in asthma [56,57]. The gene discussed is HDAC2; the disease is asthma.