Clearly, small-molecule activators of EPAC1 have the ability to induce SOCS3 and inhibit proinflammatory IL-6 signalling in VECs and suppress the proliferation of VSMCs, an event normally associated with neointima formation, and therefore may form the basis of novel therapeutic agents to combat the localised inflammation associated with atherosclerosis and NH. Here, SOCS3 is linked to atherosclerosis.