Here, other B-ALL specific genetic alterations such as fusion genes, e.g., translocation between breakpoint cluster region and tyrosine kinase abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1) [71], activating point mutations such as NRASG12D, rearrangements in the mixed lineage leukemia gene (MLLr) [72], and aberrations in fundamental genes of B-cell development, e.g., paired box 5 (PAX5) and ikaros family zinc finger protein 1 (IKZF1) [73, 74], define B-ALL progression as well as subsequent relapse [75, 76, 74, 77]. This evidence concerns the gene IKZF1 and precursor B-cell acute lymphoblastic leukemia.