In this context, it is interesting to note that spontaneous apoptosis of neutrophils is inhibited in patients with sepsis, systemic inflammatory syndrome (SIRS), and acute respiratory distress syndrome (ARDS) by the action of various pathogen- and host-derived substances, such as bacterial products (i.e., Gram-negative lipopolysaccharide; LPS), cytokines, and chemokines (i.e., IL-1β and IL-8) [3, 5–8]. Here, IL1B is linked to acute respiratory distress syndrome.