At CNV level, the chr12 alterations further impacted the expression level of the TFs ZNF384 and FOXJ2, representing previously identified fusion partners in B-ALL [85], the RNA binding factor YBX3 previously linked to pre-B cell expansion [86], the chromatin remodeling complex subunit CHD4 reported to control lineage-switching and drug resistance in leukemia [87, 88], the lysine demethylase KDM5A linked to oncogenic functions and drug tolerance [58, 89], and two Polycomb repressive complex subunits, AEBP2 and PHC1 involved in B cell maturation and ALL [90]. Here, PHC1 is linked to precursor B-cell acute lymphoblastic leukemia.