Moreover, concomitant mutation patterns have been identified in a non-recurrent manner during the evolution of the disease, affecting genes involved in pathways associated with clonal hematopoietic expansion, such as signaling pathways (JAK2), DNA methylation (DNMT3A and TET2), epigenetic regulation (ASXL1), splicing (SRSF2), transcriptional factors (ETV6), and tumor suppression (TP53) [136]. This evidence concerns the gene TET2 and neoplasm.