Two critical gaps distinguish our work from these prior studies: first, the tissue-specific regulatory mechanisms of miR-26a-5p differ across organs—lung fibrosis and retinal inflammation involve distinct cell types (e.g., alveolar epithelial cells, retinal Müller cells) and pathways (e.g., EMT, NF-κB) that are not the core drivers of skin wound healing (which relies on inflammation resolution, angiogenesis, and extracellular matrix (ECM) synthesis). Here, NFKB1 is linked to pulmonary fibrosis.