We have previously demonstrated that specific calpain inhibition reduced inflammation, cardiovascular and kidney lesions induced by angiotensin II infusion10. CalpTG mice had a reduced response to angiotensin II signalling and impaired NF-κB activation in kidney and heart tissue10. Scalia et al. evidenced that calpains are involved in the endothelial adhesion molecule expression in response to angiotensin II/AT1R signalling through the degradation of I-κB and, hence, the upregulation of NF-κB20. Furthermore, a pivotal role for calpains in mediating angiotensin II-induced atherosclerosis has been demonstrated21. Overexpression of calpastatin in bone marrow-derived cells attenuated significantly angiotensin-II induced inflammation and suppressed macrophage migration and adhesion properties. These studies evidence that the renin angiotensin system (RAS) promotes kidney and vascular lesions through a calpain dependent mobilisation of inflammatory cells, independently from alteration of blood pressure22.