For example, inflammation triggered by trauma or infection may produce a large amount of NETs, promoting the exposure of self‐antigens and inducing the NETs‐CD44‐IL‐17A pathological feedback.[38] Additionally, a specific neutrophil subset (NEU_C3_S100A12) observed in BU patients contributes to NETs formation and may also serve as a trigger for this cycle. This evidence concerns the gene IL17A and infection.