To gather mechanistic information on the role of PRMT5 and E2F1 in NB, we chose to focus our experiments on the two cell lines which represent the extreme of each expression condition: CHP‐134, with high expression levels of MYCN, PRMT5 and E2F1, and GI‐ME‐N with correspondingly lower expression levels (Fig. 1A,B), and where the effect of PRMT5 inhibition on cell viability exhibited a 6000‐fold difference (5 nm compared to 30 μm IC50, respectively; Table S2). This evidence concerns the gene E2F1 and neuroblastoma.