Nearly 20% of relapsed ALL specimens contain mutations in CREB-binding protein (CREBBP), a genetic deficit associated with changes in histone acetylation/deacetylation5, and cases of relapsed ALL have also been associated with mutations in KRAS, 5′-nucleotidase, cytosolic II (NT5C2), phoshoribosyl pyrophosphate synthetase 1 (PRPS1), NRAS, fms-related tyrosine kinase 3 (FLT3) receptor, and PTPN116–9. This evidence concerns the gene CREBBP and acute lymphoblastic leukemia.