On the other hand, the present findings suggest that the amelioration of sepsis and endotoxemia by preconditioning [26] or ischemia [27] may result from upregulation of the PK3/Akt-PKB signaling pathways [3,28-32], which directly increases [Ca2+i available for excitation-contraction coupling in cardiomyocytes. The gene discussed is AKT1; the disease is serum lipopolysaccharide activity.