Using the CRISPR KO-mediated target PTEN efficiently diminished PTEN expression in neurons, inducing neuronal hypertrophy and altering neuronal excitation, while targeting NF1 was shown to facilitate astrocytogenesis and combined targeting of three TSGs (including PTEN, NF1 and P53) by multiplex CRISPR/Cas9 triggered the pathogenesis of glioblastoma [36]. The gene discussed is PTEN; the disease is glioblastoma.