The GATA3 risk locus appears to contribute specifically to the increased prevalence of the high-risk Ph-like subtype of ALL in Hispanic/Latino patients (59) – the noncoding GATA3 variant rs3824662 was associated with minimal residual disease after induction therapy (75) and was recently demonstrated to have a functional role in the development of CRLF2 rearrangements that frequently drive the Ph-like ALL phenotype (76). This evidence concerns the gene CRLF2 and acute lymphoblastic leukemia.