Interestingly, glioblastoma patients with low expression levels of USP26 have a worse prognosis, which correlates with in vitro experiments where knock-down of USP26 leads to increased phospho-SMAD2, and cell migration [63]; since USP26 de-ubiquitinates and stabilizes SMAD7, this leads to downregulation of TGF-β activity. Here, SMAD2 is linked to glioblastoma.