Mechanistically, FTO increased Krüppel-like Factor 5 (KLF5) expression by demethylating m6A modification of KLF5 as well as enhancing glycogen synthase kinase-3 beta (GSK3β) signaling activation in VSMCs, and thus regulated VSMC phenotypic switching, highlighting the potential of FTO as a therapeutic target for aortic dissecting aneurysm (ADA)-associated diseases. Here, FTO is linked to aortic aneurysm.