The pharmacological inhibition of HMGB1 by glycyrrhizin, the suppression of the ERK1/2 activity, and the knockdown of Drp1, or its disturbed autophagy by chloroquine, either reversed the HMGB1-induced PASMCs’ proliferation/migration in vitro or prevented the MCT-induced PAH development in animals [58]. The gene discussed is HMGB1; the disease is pulmonary arterial hypertension.