Genetic mutation of the genes involved would help to resolve these questions, but due to the embryonic lethality of the α5 knockout, studies to date have involved teratocarcinomas (which recruit host vasculature) [17] and heterozygous or mosaic deletion of α5, neither of which fully addresses the requirement for this integrin in the vasculature of tumors [18]. This evidence concerns the gene IGKV2D-26 and teratocarcinoma.