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The mechanism by which ATRAP, a novel Ati receptor-associated protein, interferes with Ati receptor-mediated signaling remains largely uncertain. Here we showed that angiotensin II (Ang II)-induced vascular smooth muscle cells (VSMC) proliferation as well as neointimal formation by balloon injury were markedly inhibited by overexpression of ATRAP.In VSMC, Ang II stimulation increased extracellular signal-regulated kinase (ERK) activity, reaching a peak around 60 min. The activation of ERK could be strongly attenuated by ATRAP. We demonstrated an association between ERK activity and VSMC growth with Ang II stimulation. These results suggest that the Ati receptor-derived activation of ERK, plays an essential role in Angll-induced VSMC growth. The growth inhibitory effects of ATRAP might be due to interfering Ati receptor-mediated activation of ERK in VSMC growth and neointimal formation.