Although the upregulation of GILZ can alleviate inflammatory storms and improve survival during the early stage of sepsis, but not endotoxin tolerance (77), the downregulation of GILZ expression independent of GR activation abrogated LPS tolerance and increased responsiveness to LPS by enhancing ERK activity and rescuing MAPK signals, which was independent of GR activation (77). The gene discussed is NR3C1; the disease is Sepsis.