The CoViD-19 pandemic has brought attention to the importanceofPI3K, as its impact on the inflammatory response can lead to excessivescar tissue formation in the lungs, resulting in pulmonary fibrosis. This condition occurs due to the disruptionof inflammatory and pro-fibrotic signaling pathways, including thePI3K/AKT pathway, which triggers epithelial–mesenchymal transition(EMT) and extracellular matrix (ECM) deposits. Research suggests that regulating PI3K activity, especiallythe α isoform, could be beneficial in preventing and treatingpost-CoViD-19 pulmonary fibrosis.−, ,. This evidence concerns the gene AKT1 and pulmonary fibrosis.