Since some reports link the sensitivity to CHK inhibition to the dysfunction of the p53 axis in different tumor models [22, 24], we profiled our cell lines by conventional Sanger sequencing for the presence of TP53 mutations and CDKN2A deletions, (known recurrent genomic alterations in DLBCL which result in p53 axis and G1/S checkpoint dysfunction). The gene discussed is TP53; the disease is neoplasm.