SELE (selectin E) is a cell-surface glycoprotein mediating leukocyte adhesion to cytokine-activated endothelium through interaction with SELPLG/PSGL1 1. Beyond canonical immune adhesion, SELE plays multifaceted roles in disease pathogenesis. In cancer, SELE is expressed on tumor endothelial cells with a proinflammatory phenotype 1, and serves as a surface receptor on lymphatic endothelial cells where it activates the SRC-p-VEGFR3-MAPK pathway to promote lymphangiogenesis and metastasis in early-stage bladder cancer 2. SELE expression is elevated in diabetic wounds compared to non-diabetic wounds, where glycoengineered extracellular vesicles targeting SELE via sialyl Lewis X ligands enhance angiogenesis and wound healing 3. Genetic polymorphisms in SELE, particularly 128S/R and 561A/C variants, correlate with increased myocardial infarction risk, especially in Asian populations 4. The G98T polymorphism associates with hypertension susceptibility when combined with occupational stress 5. In atopic dermatitis, IL-13 neutralization normalizes SELE expression toward non-lesional levels, implicating SELE in type 2 inflammatory pathogenesis 6. TNF-α induces SELE upregulation on endothelial cells, which can be suppressed by quercetin via NF-κB inhibition 7. A rare SELE variant (rs5361) influences nasopharyngeal carcinoma susceptibility by modulating endothelial cell function 8.