These data are consistent with a report that inhibition of PI3K in vivo resulted in significant increases in circulating IL-1β, IL-2, IL-6, IL-10, IL-12, and TNF-α during polymicrobial sepsis [20] as well as in vitro studies [6] demonstrating the inhibitory effect of the PI3K/Akt pathway on release of these cytokines. The gene discussed is IL1B; the disease is Sepsis.