During IPF, damage occurs in the epithelium (1); normally, when there is a lesion, the ATII cells recover the epithelium (2). In IPF, the ATII cells respond in an aberrant manner which means that they secrete cytokines (3) that provoke migration, proliferation and differentiation of fibroblasts (4). These fibroblasts secrete extracellular matrix and change the architecture of the alveolus, causing it to lose its function. The damage to the ATII cells is progressive, and there is a change in the metabolism of PLs. During this process, fatty acids such as arachidonic acid are released, which decreases the viability of epithelial cells (5), and also increases the activity of phospholipases which produces palmitic acid that mediates scarring in the fibrotic process, prevents the regeneration of the epithelium and increases the recruitment of fibroblasts resistant to apoptosis (6). PS is important for maintaining alveolar homeostasis and inducing apoptosis of cells such as fibroblasts in which PS induces a calcium signal (7). Figure created in BioRender.com.