Cav1-deficient mice show a constitutive eNOS activation which results in increased microvascular permeability: down-regulation of Cav1 is predicted to promote uncontrolled eNOS activity, thereby facilitating tumour onset and stimulating tumour vasculature by inducing the expression of angiogenic growth factors that regulate endothelial cell growth and tubule formation [94, 95]. This evidence concerns the gene NOS3 and neoplasm.