Indeed, we found that TAC-induced pulmonary inflammation and remodeling are significantly attenuated by inhibition of IL-1β signaling with blocking antibodies (32) or inhibition of oxidative stress by isolevuglandin scavenger 2-hydroxybenzylamine (2-HOBA) significantly attenuated LV failure-induced pulmonary inflammation, fibrosis, vessel remodeling, and RV hypertrophy (33). The gene discussed is IL1B; the disease is persistent truncus arteriosus.