New research in mice has revealed that the protein talin1, which is involved in anchoring the podocyte foot processes to the basement membrane, is required for glomerular filtration barrier maintenance. Specific deletion of talin1 in podocytes resulted in reduced β1 integrin activation and podocyte cell adhesion, proteinuria, foot process effacement and profound disruption to the actin cytoskeleton in podocytes. In patients with nephrotic syndrome, talin1 cleavage seems to be associated with activation of the protease calpain; inhibition of calpain in mice following glomerular injury resulted in reduced talin1 cleavage and albuminuria, suggesting that this protease might be a viable target for future therapies.