However, recent data increasingly describe strong associations between DIL and newer agents, such as TNF inhibitors.4 By inhibiting Th1 response, anti-TNFα agents could be assumed to trigger Th2 autoimmune reactivity, including SLE.5 Pathogenic hypotheses for the ATIL syndrome include a reduced CD44 expression influencing the clearance of apoptotic neutrophils and nuclear debris by phagocytes, thereby leading to autoantibody production against nuclear antigens and DNA. Here, CD44 is linked to systemic lupus erythematosus.