Members of the integrin family play central roles in regulating not only cell adhesion and migration but also cell differentiation and signalling. Aberrant integrin expression and signalling have been observed in various pathological conditions such as tumour growth and metastasis. Changes in integrin expression patterns have also been reported in some physiological processes such as wound healing. Elucidating the precise roles of these molecules in vivo is essential for our understanding of these biological processes and diseases, and for developing strategies for inhibiting or modulating adhesive function for therapeutic applications. To this end, using integrin-deficient mice, we have focused our efforts on the functions of integrins in pathological angiogenesis and wound healing. Our work has shed significant light on the roles of avb3-integrin in angiogenesis, and the roles of both a3b1 and avb3 in wound healing. Inhibition of avb3-integrin function has been reported to suppress neovascularisation and tumour growth, suggesting that this integrin is a critical modulator of angiogenesis. Our work showed that, surprisingly, mice lacking b3-integrins not only support tumourigenesis, but even show enhanced tumour growth. Moreover, the tumours in these integrin-deficient mice display enhanced angiogenesis, suggesting strongly that b3-integrins are not essential for neovascularisation. We have demonstrated that avb3 integrin plays a key role in the control of angiogenesis by its regulation of the pro-angiogenic receptor, Flk-1.