In our sample, FLT3 mutations were not detected in patients with recurrent genetic alterations commonly associated with B-ALL, including ETV6::RUNX1, TCF3::PBX1, BCR::ABL1, r-KMT2A, P2RY8::CRLF2 rearrangements, PAX5 alterations, or deletions involving IKZF1. This finding supports the hypothesis that, contrary to the prevailing concept of kinase alterations being secondary (31, 60), FLT3 mutations may function as leukemogenic drivers in a small subset of B-ALL (5, 61). Here, BCR is linked to precursor B-cell acute lymphoblastic leukemia.