Although numerous somatic mutations that contribute to the pathogenesis of childhood acute lymphoblastic leukemia (ALL) have been identified, no specific cytogenetic or molecular abnormalities are known to be consistently associated with relapse. The p16INK4A (p16), which encodes for both p16INK4A and p19ARF proteins, and p15INK4B (p15) genes are inactivated by homozygous deletion and/or p15 pr...