These observations in DLBCL may support previous functional studies, which showed that TAp63α and TAp63γ (but not ΔNp63) could induce apoptosis at lesser levels than WT-p53 [48]; TAp63, and also TAp73, together with p53, may transactivate a group of common target genes in response to DNA damage, including damage resulting from exposure to doxorubicin, a component of R-CHOP;1 TAp63 and MUT-p53 antagonize each other mainly in the regulation of metastasis and tumor dissemination [5]; p53 mutants may bind directly to p63 and inhibit the p63-mediated transcription of p53 target genes [49, 50]. This evidence concerns the gene DDIT3 and neoplasm.