Early antibiotics treatment and effective anti‐inflammatory control is a critical element of treatment for sepsis.[26] CD38, as a type II transmembrane glycoprotein with metabolic enzymatic function, can catalyze NAD+ to nicotinamide and other metabolites.[27] While CD38 has been extensively studied as a targeted therapy for multiple myeloma,[28] recent research demonstrated that CD38 inhibition enhanced the effector function of CD8+ T cells, reversed mitochondrial defects, and improved viral clearance.[29]The roles of CD38 in primary monocytes of sepsis were not fully illustrated till now. The gene discussed is CD38; the disease is AL amyloidosis.