Among other mechanisms, E2F1 can be regulated by PRMT5 arginine methylation; it has indeed been demonstrated that the binding of cyclin A to E2F1 augments PRMT5 methylation of E2F1, thus ensuring that it is locked in a cell cycle progression mode55 Based on the observed down‐regulation of cyclin A, together with the down‐regulation of other E2F1 target genes, in PRMT5‐silenced MM cells, it could be hypothesized that the E2F1 activity in MM is affected by PRMT5‐mediated arginine methylation. Here, PRMT5 is linked to Miyoshi myopathy.