Mechanistically, these optimized effects were associated with enhanced the adenosine (cAMP)‐protein kinase A (PKA) pathway, which upregulated phosphorylate‐phospholamban (p‐PLN) (Ser16) and promoted sarco/endoplasmic reticulum Ca2+ ATPase (Serca) and Ryanodine Receptor 2 (RyR2) expression in the sarcoplasmic reticulum (SR), and ultimately restored Ca2+ handling in response to sepsis. The gene discussed is ATP2A3; the disease is Sepsis.