Unexpectedly, we observed that neither PELI1 knockdown nor overexpression affected IR‐induced activation of canonical NF‐κB (including p65, p50 and c‐Rel that highly expressed in B and T lymphocytes) and AKT signaling, two well‐known pathways that mediate tumor cell apoptosis, in the TE‐1 and ECA‐109 cells (Fig. S4A,B). This evidence concerns the gene AKT1 and neoplasm.