Using a mouse model, treatment with class I (MS-275) or class IIa (MC-1568) HDAC inhibitors decreased the incidence of AAA, macrophage inflammation, and pro-inflammatory mediators, partly due to decreased MMP-2 and MMP-9 activity following HDAC inhibition (Galán et al., 2016). The gene discussed is MMP9; the disease is triple-A syndrome.