NQO1 gene is a member of the NAD(P)H dehydrogenase (quinone) family and encodes a cytoplasmic 2-electron reductase. NQO1 forms homodimers and reduces quinones to hydroquinones. NQO1's enzymatic activity prevents the one-electron reduction of quinones that results in the production of radical species. Mutations in the NQO1 gene have been associated with tardive dyskinesia (TD), an increased risk of hematotoxicity after exposure to benzene, and susceptibility to various forms of cancer. Altered expression of NQO1 has been seen in many tumors and is also associated with Alzheimer's disease (AD). Alternate transcriptional splice variants, encoding different isoforms, have been characterized. Recent pharmacological research suggests the feasibility of genotype-directed redox chemotherapeutic intervention targeting NQO1 breast cancer, a common missense genotype encoding a functionally impaired NQO1 protein.

D-tyrosyl-tRNA(Tyr) deacylase 1(DTD1) belongs to the DTD family, and expressed in many adult and fetal tissues such as testis, ovary, spleen in adult and fetal brain. It is a nucleus and cytoplasm located protein, and is preferentially phosphorylated in cells arrested early in S phase. DTD1 is an ATPase involved in DNA replication, it may facilitate loading of CDC45 onto pre-replication complexes. The protein may hydrolyze D-tyrosyl-tRNA(Tyr) into D-tyrosine and free tRNA(Tyr), a possible defense mechanism against a harmful effect of D-tyrosine.