Further analyses of relevant data on pre-, and post-natal development and childhood cancers [e.g., neuroblastoma, B-lineage infant acute lymphoblastic leukemia (ALL), mixed lineage leukemia (MLL), myeloid leukemia-Downe syndrome-ML-DS or medulloblastoma] suggest rapid aging or maturation of prenatal-embryonic tissues, accompanied by increased genomic mutations and progressive genomic instability and fusion, presenting embryonic hyperplastic cell growth patterns that favor abnormal proliferations of cell survival under hypoxic conditions [155–159]. Here, KMT2A is linked to acute lymphoblastic leukemia.