In B-ALL, the most common pathogenic pathways are RAS signaling (~ 48%, NRAS, KRAS, PTPN11, FLT3, NF1, etc.)and Lymphoid development/differentiation (18–80%, PAX5, IKZF1, EBF1, etc.)2, 20, 21, and we found a similar distribution of genetic changes in this study (42% RAS signaling and 49% Lymphoid development/differentiation variants were identified). This evidence concerns the gene EBF1 and precursor B-cell acute lymphoblastic leukemia.