Thus, we examined that the loss of USPNL markedly enhanced the ubiquitination activity of EGFR in GBM cells transfected with shUSP6NL compared with the control (NT) (Figure 6F), and the results indicated that USP6NL may play a vital role in the protection and accumulation of EGFR by promoting its deubiquitination and preventing its subsequent downregulation. The gene discussed is USP6NL; the disease is glioblastoma.