As shown in Fig. 3, we observed that at day 3 post sepsis, infiltrating monocytes within the heart underwent robust exhaustion reflected in pathogenic inflammation (elevated Cd38, Bst1, ItgaM) and immune suppression (reduced Cd86, and elevated Cd274), as well as reduced differentiation and enhanced proliferative potential (elevated Stmn1). The gene discussed is CD38; the disease is Sepsis.