TP53 mutations displayed a significantly increased frequency and MYD88 (0/53), NFKBIE (4/53) or CD79B (4/53) mutations were less or not found in our pGI-DLBCL cohort, suggesting that the pathogenesis of pGI-DLBCL were different from the nodal or other extranodal DLBCL, which relies on an activated NF-κB signaling pathway due to the common mutations in the above mentioned MYD88, NFKBIE, or CD79B genes [26]. This evidence concerns the gene TP53 and diffuse large B-cell lymphoma.