Interestingly, CaMK4 controls the activation of the NLRP3 inflammasome in Type II alveolar epithelial cells during LPS‐induced ALI, and its inhibition could be a therapeutic approach for ALI.[41, 42] As CaMK4 plays a crucial role in the Calhm6‐CaMK4‐Chp1 axis, we hypothesize that early infection triggers ATP release via Calhm6, which in turn contributes to inflammasome activation and host defense through CaMK4 regulation. The gene discussed is CAMK4; the disease is acute respiratory distress syndrome.