The increased mutational burden observed in genes such as BCL2, CD83, MYC exon1, IRF8, PAX5-SE, PIM1, RHOH/TTF, and TCL1A during idelalisib treatment and BIRC3, BTG2, LRMP during ibrutinib treatment mirrors the known spectrum of AID activity described in CLL and diffuse large B-cell lymphoma, where AID is responsible for widespread, off-target deamination events that contribute to tumor evolution [27]. The gene discussed is AICDA; the disease is neoplasm.