CLDN5 and neoplasm: This mechanism was corroborated by a similar finding in melanoma that tumor-secreted cANGPTL4 disrupts endothelial cell–cell junctions by directly interacting with integrin α5β1, VE-cadherin, and claudin-5, thereby promoting vascular leakiness in the tumor microenvironment—a phenomenon that facilitates lung metastasis [75].