Some typical anomalies useful in a clinical setting for B-ALL, in addition to hyperdiploidy and hypodiploidy, are the translocations t(9;22)(q34;q11.2) (BCR-ABL1) [15], t(12;21) (p13;q22) (ETV6-RUNX1) [16], t(1;19) (q23;p13.3) (TCF3-PBX1) [17], and t(5;14) (q31;q32) (IGH-IL3) [17]; the rearrangement t(v;11q23) (MLL); the intrachromosomal amplification of chromosome 21 (iAMP21) [18]; and the deletion of CDKN2A/B [19]. This evidence concerns the gene RUNX1 and acute lymphoblastic leukemia.