Notably, activation of ILK, which links F-actin to focal adhesions and is required for integrin-mediated force generation, sustains nuclear YAP accumulation in pulmonary arterial vascular smooth muscle cells to promote cell proliferation in pulmonary arterial hypertension, a disease characterized by increased deposition of extracellular matrix and vascular stiffness (Kudryashova et al., 2016). This evidence concerns the gene ILK and pulmonary arterial hypertension.