More and more evidence has shown Ash2l can regulate inflammatory response and vascular function, for example, our previous study showed Ash2l aggravated fibrosis and inflammation through HIPK2 transcriptional activation in diabetic nephropathy [26]; and aberrant histone methylation of IFN-γ associating H3K4me3 and H3K27me3 caused by over-binding of Ash2l and JMJD3 might be involved in vascular damage in Kawasaki disease in the acute phase [27]. This evidence concerns the gene IFNG and Kawasaki disease.