YTHDF3 and triple-A syndrome: Besides, the specific inhibitor of YTHDF3 expression may act as a modulator of macrophage M2 polarization adaptation, which would reduce the secretion of matrix metalloproteinases, promote the repair process of the aortic wall, and alleviate vascular inflammation by downregulating the expression levels of pro-inflammatory cytokines such as IL1β and TNF, and upregulating the secretion of anti-inflammatory cytokines and chemokines such as IL10 and TGFβ, suggesting that YTHDF3 is a potential therapeutic target for AAA (74, 81).