Exposure of ECs to proinflammatory stimulus with LPS, TNF-α, or IL-1β upregulates ICAM-1 and VCAM-1 expression, as a natural process for lymphocyte recruitment and infiltration (50, 51); however, dysfunctional expression of adhesion molecules, such as ICAM-1, reduces T cell adhesion to tumor endothelium, likely due to microenvironmental cues that reprogrammed ECs, making it harder to mount an anti-tumor immune response (47, 52, 53). Here, ICAM1 is linked to neoplasm.