In the two patients who underwent ASCT (MC3 and MC205), genetically and transcriptionally different subclones were present before treatment, and some subclones expanded in the relapse tumor through the acquisition of additional mutations (CDKN2A, exemplified by MC3) or altering their transcriptomic expression after migrating into different tissues (exemplified by MC205). Here, CDKN2A is linked to neoplasm.