Collectively, these findings identify PRMT5 as a critical regulator of the FA pathway in glioblastoma and demonstrate that PRMT5 inhibition potentiates TMZ efficacy by disrupting FA-dependent homologous recombination repair, indicating that the combination of PRMT5 inhibition and TMZ could be a novel therapeutic strategy for glioblastoma. The gene discussed is PRMT5; the disease is glioblastoma.