However, interleukin-33 (IL-33) has therapeutic potential in view of its capacity to antagonize the TLR4-dependent modulation of interrelated GRK2 and CXCR2 activities in a mouse model of sepsis and in human neutrophils [160], as also suggested for fibrates, which are ligands of peroxisome proliferator-activated receptor-alpha [161]. The gene discussed is CXCR2; the disease is Sepsis.