BCL2 and neoplasm: From this PCA, we identified a DLBCL AICDA-high methylation signature (n = 37,557 DLBCL AICDA-perturbed CpG; Supplementary Fig. 6c) that exhibited similar methylation dynamics to VavP-Bcl2+Aicda (and opposite to Aicda−/− GC B cells), including loss of CpG methylation from intermediate and highly methylated states (Fig. 4b) alongside gain of inter-tumor methylation heterogeneity (Fig. 4c).