The findings from animal models and in vitro experiments indicated that TAC causes early cardiac neutrophil infiltration, and the highly expression of S100A8 and S100A9 in these neutrophils triggers acute inflammation and adaptive cardiac hypertrophy possibly through p38 MAPK/JNK/AP-1-mediated production of IL-1β and CCL2 and CCL6. The gene discussed is JUN; the disease is persistent truncus arteriosus.