Therefore, we used GECs as a reliable model of GBM angiogenesis, and we proceeded with the examination of calpain expression in GECs, revealing an upregulation of the most active calpains, CAPN1 and CAPN2, and their small regulator subunits (CAPNS1 and CAPNS2), together with a downregulation of CAST, their endogenous inhibitor. This evidence concerns the gene CAST and glioblastoma.