Although it is well-documented that plasma norepinephrine levels are significantly elevated in the setting of sepsis [16] and norepinephrine alone can directly stimulate cardiomyocyte apoptosis by activating the β-adrenoceptor (AR) [17,18], little is known about the causative contribution of endogenous norepinephrine in sepsis-induced cardiomyocyte apoptosis. This evidence concerns the gene AR and Sepsis.