While SOCE interplay with RTK activity has not been examined in GBM, work performed with a variety of other cancer cell lines offered the tantalizing result that disruption of EGFR/ErbB2 signaling produces an important decrease in SOCE signal amplitude—a finding suggesting that the anticancer effects of RTK inhibitors may be mediated by inhibition of SOCE [248]. This evidence concerns the gene EGFR and glioblastoma.