Likewise, infection and cellular stress can enhance inflammasome activation in the activated macrophages as indicated by redistribution and spatial organization of ASC (apoptotic speck-like protein containing a CARD) to the cytoplasm, followed by assembly of inflammasome components, including Nod-like receptors (NLR) and caspase-1 in the perinuclear space, which is necessary for inflammasome function such as maturation of IL-1β and IL-18 for further inflammatory signaling. This evidence concerns the gene IL1B and infection.