Further investigations suggested a role for PRMT1 in these interactions, and it was found that Myc was both symmetrically (by PRMT5) and asymmetrically (by PRMT1) dimethylated in GBM stem cells and that these modifications were required for Myc activity and turnover, respectively (Favia et al. 2019). The gene discussed is PRMT1; the disease is glioblastoma.