This inferred context-dependence of target function provides a hypothetical molecular framework for investigating its potential application across fibrotic diseases: AKT1 inhibition blocks PI3K-mTOR to reduce hepatic collagen synthesis (77), and EGFR targeting suppresses PDGFR-β autophosphorylation to inhibit alveolar EMT(78), synergizing with CKD’s ECM remodeling. Here, EGFR is linked to chronic kidney disease.