Our findings are supported by earlier studies that showed the potent ability of Prist to modulate NF-κB activation and subsequently to ameliorate the production of pro-inflammatory mediators in chronic obstructive pulmonary disease [54], LPS-induced inflammation [55], and doxorubicin-induced cardiotoxicity [56]. The gene discussed is NFKB1; the disease is chronic obstructive pulmonary disease.