SELE and atherosclerosis: Functional analysis in cellular models via the CRISPR/dCas9-Dnmt3a system revealed that DNA methylation at three genes (TRIM6, FLRT2, and TLN2) harboring the aberrantly methylated probes could regulate the expression of three endothelial cell adhesion markers (i.e., ICAM1, VCAM1, and SELE) and thus be functionally implicated in endothelial cell activation and leukocyte transendothelial migration [28], one of the mechanisms underlying atherosclerosis [29, 30] and stroke [31].