It has been demonstrated that augmented levels of Receptor Interacting Serine/Threonine Kinase 3 (RIPK3) and phosphorylated MLKL in alveolar epithelial cells (AECs) in IPF lungs46 leading Lee et al. to postulate that cell-damaging agents injure AECs, leading RIPK-3–regulated necroptosis. The gene discussed is MLKL; the disease is idiopathic pulmonary fibrosis.