Interestingly, lack of RIPK1 kinase activity, and to a lesser extent RIPK3 deficiency, limited the activation of TH17 cells, which is associated with more severe asthma endotypes,2 in FADDAEC-KO mice, suggesting that in the context of type 2 immunity in the lung, AEC necroptosis might potentiate neutrophil-associated TH17 pathogenic responses. The gene discussed is RIPK1; the disease is asthma.