NLRP3 and acute respiratory distress syndrome: 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.