In conclusion, ABI-171 represents a promising disease-modifying therapy for IPF by addressing multiple pathological processes, including inflammation, fibroblast activation, EMT, and ECM remodeling through the dual inhibition of DYRK1A and PIM1 kinases, as well as LOXL2 and TGF-β signaling inhibition. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.