Furthermore, it has already been shown that the extent of erlotinib-mediated suppression of anchorage-independent growth of glioblastoma-derived cell lines is inversely correlated with the cellular capability to induce EGFR/HER1 messenger ribonucleic acid (mRNA), highlighting the important role of EGFR/HER1 in the pathogenesis of glioblastoma [81]. The gene discussed is EGFR; the disease is glioblastoma.