Pediatric Lymphoid neoplasms are the largest group of tumors in children, comprising approximately one-third of all pediatric cancers. The high incidence of these tumors in children is likely due to the active development of the adaptive immune system against microbes during the early stages of life. Adaptive immunity produces specific antibodies that target microbes through genomic events such as V(D)J recombination, class-switch recombination (CSR), and somatic hypermutation (SHM). However, these genomic manipulations can also cause off-target genomic instability and resulting malignancy, with a majority of acute lymphoblastic leukemias and lymphomas associated with chromosomal abnormalities that bear the hallmarks of aberrant V(D)J or CSR.^1,2 Detection of these aberrant genomic rearrangements involving Immunoglobulin (IG) and T-cell receptor (TCR) genes is important for both diagnostic and risk stratification purposes in clinical settings.