This mode of tumor blood supply, which differs from traditional vascular endothelial angiogenesis, offers a novel approach for targeted tumor therapy.[9–12] In recent years, some key pathways and related mechanisms of VM have been reported, among which VE-cadherin and EphA2 are the first 2 proteins identified for VM formation, playing a crucial role in the vascular signaling pathways that contribute to VM.[13] In melanoma, malignant melanoma initiation cells contribute to VM formation through the expression of ATP-binding cassette (ABC) member ABCB5. Here, EPHA2 is linked to neoplasm.