In support of the hypothesis that, in sepsis, Th2 predominance arises from a shift from Th1 to Th2-biased cell proliferation, Brunner et al. [21] showed an increase in the levels of soluble suppressor of tumorigenicity (sST2), a member of the interleukin-33 (IL-33) family. This evidence concerns the gene IL33 and Sepsis.