Overall, prior to understanding whether using a BTLA antagonist is a viable option for the treatment of critically ill patients, additional studies are needed to elucidate whether the augmented BTLA expression that we observed on the septic and SIRS patient and mouse CD4+ T cells indeed inhibits their function (including ex vivo cytokine production and upregulation of activation markers, such as CD69 and CD25), proliferation, or differentiation. The gene discussed is CD69; the disease is systemic inflammatory response syndrome.