Mounting evidence links SOCE in MCs to extracellular matrix protein synthesis and deposition.59–62 Changes in SOCE parallel mesangial expansion and the fibrotic glomerular phenotype in DN.52,61 Moreover, PAR1 overactivation and high activity of serine proteases have recently been linked to glomerular pathologies like FSGS and DN.24,55 Interestingly, the above-mentioned studies emphasize the key role of TRPC6 channels in PAR1-mediated podocyte and glomerular damage. This evidence concerns the gene TRPC6 and liver dysplastic nodule.