MLKL and Sepsis: To establish an ex vivo model of RIPK1‐dependent signaling, we stimulated MLE‐12 alveolar epithelial cells with LPS (1μgmL−1, 24 h), a pathogen‐associated molecular pattern (PAMP) implicated in sepsis pathogenesis.[32, 33, 34] This treatment induced significant RIPK1/RIPK3/MLKL activation (Figure S1H, Supporting Information), confirming LPS as a potent driver of RIPK1‐mediated inflammatory cascades in pulmonary epithelium.