Background
Methotrexate (MTX) remains a critical component in the treatment of pediatric acute lymphoblastic leukemia (ALL), exerting its antileukemic effect through interference of the folate metabolic pathway. MTHFR is an enzyme that serves as the rate limiting step within this pathway and there has been speculation that certain MTHFR single nucleotide polymorphisms (SNPs) alter physiologic responses to MTX and affects drug toxicity.