Therefore, in pulmonary diseases characterized by neutrophil accumulation and excessive inflammation, loss of IL-1β bioactivity may be useful in modulating pulmonary inflammatory diseases, potentially without increasing the risk of serious adverse secondary effects such as pulmonary infections which are seen in rheumatoid arthritis (RA) and Crohn's disease (CD) patients using anti-TNF-α therapeutic agents. This evidence concerns the gene IL1B and lung disorder.