LUBAC facilitates aberrant somatic hypermutations mediated by AID. (A-C) Mutations with VAF >0.05 in tumor samples were selected and analyzed. (A) Venn diagram depicting the overlap between genes recurrently mutated in lymphoma cells derived from CD19-cre-HOIP/MYD88LP mice and murine homolog of known or predicted targets of aberrant somatic hypermutation mediated by AID.³⁰  (B) Numbers of SNVs at C/G within the WRCY/RGYW motifs (left), and numbers of C:G (center) and transition mutations (right) in each tumor sample. (C) Mutation distribution in targeted genes observed in lymphoma cells derived from 8 CD19-cre-HOIP/MYD88LP mice. Shadows indicate the 2-kb region downstream of the transcription start site (TSS). (D) Numbers of nonsynonymous mutations in each human DLBCL sample. (E) Numbers of SNVs at C/G within the WRCY/RGYW motifs (left), and numbers of C:G (center) and transition mutations (right) in each human DLBCL sample. (D and E) Average fold change of FPKM (high vs low) = 1.36. Boxes represent the median and the first and third quartiles, and whiskers represent the minimum and maximum of all data points. *P < .05, **P < .01, and ***P < .001, Fisher’s exact test (A), Brunner-Munzel test (B), or 2-tailed unpaired Student t test (D and E). See also supplemental Figure 3 and supplemental Tables 6-8.