A, In wild-type (Mgp+/+) aortic tissue, MGP represses TGFβ production in VSMCs, Wnt16 is abundant, and Notch signaling is active supporting a stable, contractile phenotype of VSMCs. B, In the aortae of MGP-null (Mgp−/−) mice, TGFβ production is elevated leading to down-regulation of Wnt16 and repression of Notch signaling, and allowing for chondrogenic transformation of VSMCs by additional TGFβ-mediated events.