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The parent Tβ4 protein forms a 1:1 complex with G-actin and prevents its polymerization into F-actin filaments (Safer, Elzinga & Nachmias, 1991), and Tβ4 binding measurably alters monomer conformation and dynamics (De La Cruz et al., 2000)

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However, under risk factors such as hemodynamic changes, hypercholesterolemia, hypertension, diabetes, and smoking, endothelial cells transition from an anti-inflammatory and anticoagulant state to a pro-inflammatory and pro-thrombotic state