Therefore, our study of non-septic CAP patient monocytes provides benchmark evidence that the phenomenon of endotoxin tolerance is not exclusive to sepsis and lends further weight to challenge the current paradigm that endotoxin tolerance is a pathophysiological mechanism which dampens pro-inflammatory mediators (e.g., TNF, IL-1β, IL-6) while activating anti-inflammatory factors such as IL-10. The gene discussed is IL1B; the disease is Sepsis.