The lack of p53 increase upon HEATR1 inhibition is not due to GBM cells being unable to activate RPL5/RPL11-MDM2-p53 signalling as low ActD dosage, which leads to the pathway activation (Holmberg Olausson et al, 2012), results in robust p53 accumulation (Appendix Fig. S6C). The gene discussed is HEATR1; the disease is glioblastoma.