Interestingly, we showed that HDM‐driven neutrophilic airway inflammation in mice carrying Tnfaip3‐deficient cDCs was independent of IL‐17, supporting the concept that neutrophilic airway inflammation in asthma models can be IL‐17‐independent and may involve Th1 cells or HMGB1‐producing ILC2s. This evidence concerns the gene TNFAIP3 and asthma.