They first showed that α-TOS promoted beast cancer dormancy in an immunocompromised mouse (Malafa and Neitzel, 2000) and, later on, also melanoma dormancy (Malafa et al, 2002b); in both cases, inhibition of angiogenesis via suppression of VEGF signalling by α-TOS was suggested as the underlying mechanism, pointing to an indirect effect of the VE analogue on cancer growth. This evidence concerns the gene VEGFA and cancer.