However, translational work completed by Artlett and colleagues demonstrated the connection between NLRP3 inflammasome activation and SSc by showing that dermal fibroblasts from SSc patients exhibit increased expression of inflammasome components, and that experimentally induced caspase-1 inhibition of both dermal and lung SSc fibroblasts ameliorated collagen deposition, reduced IL-1β and IL-18 secretion, and decreased αSMA (alpha smooth muscle actin) expression (Artlett et al., 2011). The gene discussed is IL1B; the disease is systemic sclerosis.