In this study, PRMT5 activity (but not expression) was upregulated in response to mTOR inhibitors (rapamycin or PP242). Furthermore, it was revealed that in response to mTOR inhibition, the activated PRMT5 dimethylated hnRNPA1, which resulted in stimulation of hnRNPA1 binding to cyclin D1 and c-MYC internal ribosome entry site (IRES) RNAs. This promoted mRNA translation of the latter two, resulting in drug resistance in glioblastomas. Here, MYC is linked to glioblastoma.