In line with the past studies, we found that FL tumour cells had a number of mutations in addition to BCL2/IGH rearrangement, and that recurrent variants were enriched in genes associated with epigenetic regulation, BCR signalling, B cell development, immune responses, and programmed cell death, and defined CREBBP and TNFRSF14 as driver mutations in our overall cohort. Here, CREBBP is linked to neoplasm.