As these processes were shown to be p53‐activation/caspase 3 cleavage dependent,41 we did not expect them to be induced by DMOG treatment, which is known to inhibit PHD3‐mediated hydroxylation of p53, preventing its accumulation and apoptotic activity.18 Indeed, when we explored the impact of DFO and DMOG treatment on DNA damage, reflected by DDR, in MCL cell lines, visible increase of γH2AX signal indicative of DDR was detected in cells treated with DFO, but not in cells treated with DMOG (Figure 5). The gene discussed is EGLN3; the disease is mantle cell lymphoma.