In hematologic cancer models, such as MLL-fusion leukemia [46], acute myeloid leukemia (AML) [47], Burkitt's lymphoma [48], multiple myeloma [49], and B-cell acute lymphoblastic (BLL) leukemia [50], amplification of onco-protein Myc drives distinct transcription programs, and leads to a consequence of cell proliferation. This evidence concerns the gene KMT2A and AL amyloidosis.