Alternative mechanisms for tumor suppressor pathway inactivation may be involved in the pathogenesis of near-haploid B-ALL; for instance, microdeletions of CDKN2A/B loci on chromosome 9, typically monosomic in near-haploid B-ALL, are common in this hypodiploid subtype [30]. The gene discussed is CDKN2A; the disease is precursor B-cell acute lymphoblastic leukemia.