IL1B and Sepsis: Traditionally, the physiopathology of sepsis is attributed to a hyperinflammatory response, the ‘cytokine storm', that can directly lead to death or favor the insurgence of an immunosuppressive phase during which multiple organ dysfunction occurs.1 We have recently reproduced in vitro on primary monocytes the cytokine storm: the simultaneous activation of multiple Toll-like receptors (TLRs) results in oxidative stress responsible for a marked enhancement of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) secretion.7