CAECs support breast and melanoma tumor growth both by promoting tumor vasculature essential for nutrient and oxygen delivery and by favoring the recruitment of immunosuppressive rather than effector immune cells through the downregulation of adhesion molecules such as the ligands ICAM1 (intercellular adhesion molecule 1) and VCAM1 (vascular cell adhesion protein 1), which promote T cell extravasation into the TME by binding to LFA1 (antigen 1 associated with lymphocyte function) and VLA4 (very late antigen 4) on T cells [57]. The gene discussed is VCAM1; the disease is melanoma.