Hamidi et al. described an increased susceptibility to death from endotoxemia, while Abad et al. found that VIP-KO mice exhibit resistance to endotoxic shock and decreased pro-inflammatory responses due, in part, to the presence of an intrinsic defect in the responsiveness of inflammatory cells in the chronic absence of VIP, suggesting that these mice may exhibit a defect in the innate arm of the immune system [104,105]. The gene discussed is VIP; the disease is serum lipopolysaccharide activity.