Based on our findings that treatment with a phosphatase inhibitor completely restored the ERK phosphorylation that had been in the VSMCs from defeated mice and that it augmented MKP-1 gene and protein expression in the perivascular area after CaCl2 application in the defeated mice, it is likely that the RSD-induced modulation of the MAPK–MKP-1 pathway in VSMCs is implicated in the impaired migration and replication of α-SMA-positive cells, thereby contributing to the decreased fibrotic wound healing process and subsequent AAA expansion in defeated mice. Here, ACTA1 is linked to triple-A syndrome.