Our experiments showed that inhibition of RIPK1 kinase activity, by crossing to mice expressing kinase-inactive RIPK1, as well as RIPK3 or MLKL deficiency greatly attenuated the severity of airway inflammation in FADDAEC-KO mice, suggesting that RIPK1-RIPK3-MLKL-mediated necroptosis of FADD-deficient AECs strongly contributes to the exacerbation of HDM-induced asthma. The gene discussed is MLKL; the disease is asthma.