As shown in Fig. 4b, αSMA+CD68+, αSMA+RUNX2+, αSMA+CD34+, and αSMA+LUM+ cells were induced under AAA condition, and reversed by FAM3A overexpression mediated by adenovirus, suggesting the roles of FAM3A in suppressing VSMC transdifferentiation toward other intermediate cell types in vivo. Here, ACTA1 is linked to triple-A syndrome.