Firstly, ATP11A is cleaved during apoptosis and results in phosphatidylserine’s translocation to the outer leaflet of the cell membrane, which is an “eat me” signal during efferocytosis.83–86 Increased apoptosis of epithelial cells and resistance to apoptosis in myofibroblasts are hallmarks of IPF, correlating with aberrant collagen deposition.87,88 During IPF, we speculate that increased ATP11A may contribute to impaired efferocytosis, an observation reported in murine models89 and IPF patient samples90. The gene discussed is ATP11A; the disease is idiopathic pulmonary fibrosis.