Consistent with the suggestion that targeting USP6NL enhanced β-catenin ubiquitination suppressed cancer cell proliferation and induced cell cycle arrest in colorectal cell lines [23], as well as considering that EGFR is the most commonly mutated driver of oncogenicity in patients with GBM, there was hope for targeting EGFR with inhibitors; unfortunately, this showed no or very little response toward treatment [28]. The gene discussed is EGFR; the disease is glioblastoma.