These findings are consistentwith emerging in vivo evidence that PFAS can activateTGF-β/Smad pathways and promote fibrotic tissue remodeling. In addition, epidemiologic data have linkedPFHxS levels to increased odds of liver fibrosis. Since myocardial fibrosis can disrupt electrical conductivityand relaxationraising the risk of arrhythmias and diastolicdysfunction, future study is needed tofurther analyze functional consequence including contractility associatedwith the proteomic changes in ECM organization and metabolism. The gene discussed is PFAS; the disease is Myocardial fibrosis.