Utilization of a β1-AR blocker, CaMKII inhibitor, and β1-AR agonist showed that the NE from ICA cells can active cardiac β1-AR-CaMKII signaling, which crosstalks with NF-κB and MAPK pathways to promote TNF-α production and myocardial dysfunction during sepsis. The gene discussed is NFKB1; the disease is Sepsis.