MYD88 mutations and high expression of BCL2 are enriched in ABC-DLBCL. (A) MYD88 mutations are substantially enriched in human ABC-DLBCL. Human DLBCLs were stratified as ABC- or GCB-DLBCL following the Hans algorithm, as depicted in (B). After immunohistochemistry-based stratification, DNA was isolated from tissue sections and subjected to targeted deep sequencing by a multiplex PCR, which covered the ATM, BTK, CD79B, DDX3X, FBXW7, MAPK1, MYD88, NOTCH1, PIK3CA, PIK3CD, PTEN, PTPN6, SF3B1, TP53, and XPO1 genes. MYD88 mutations per se, and particularly the MYD88^p.L265P mutation were substantially enriched in ABC-DLBCL. Similarly, CD79B and PTEN mutations were enriched in ABC-DLBCL. (C) Distribution of MYD88 mutations detected in human DLBCL samples is shown in pie charts. The samples were classified into high and low or negative expression of BCL2, as shown in (D). (E) High protein expression levels of BCL2 are significantly enriched in ABC-DLBCL (Fisher’s exact test).