VASH1 and carcinoma: However, human patients suffering from a broad range of carcinomas had mutations in VASH1 and VASH2 that compromised their tubulin detyrosination activity [17] and, more recently, it was suggested that the MT detyrosinating activity of VASH1 inhibited angiogenesis by interfering with endocytosis and trafficking of proangiogenic factor receptors [134].