Cause
While the specific causes of TOF have not been fully identified, there are various environmental or genetic factors that have been associated with TOF. So far, around 20% of overall CHD cases have been due to known causes such as genetic defects and teratogens which are various factors causing embryo development abnormalities or birth defects. However, the other 80% of cases have little known about their cause.Genetic factors linked to TOF include various gene mutations or deletions. Gene deletions associated with TOF include chromosome 22 deletion as well as DiGeorge syndrome.Specific genes associations with TOF include:

JAG1 codes for ligands within the Notch family of proteins and is highly expressed in the developing heart. Mutations of the JAG1 gene can lead to abnormal heart development associated with TOF. NKX2-5 codes for cardiac morphogenesis regulators to allow for proper heart development. Defects in this gene typically causes septal defects and has been associated with around 4% of all TOF cases. ZFPM2 is another cardiac regulator involved in regulation of GATA4. Mutations of the ZFPM2 gene lead to reduced GATA production and have been seen in some TOF cases. VEGF a well-known endothelial growth factor involved in the vascularization of the heart. Decreased VEGF expression has been shown to be a modifier of TOF. NOTCH1 is involved in the vascularization of tissues and is the most common site of genetic variations involved with TOF, accounting for 7% of all TOF cases. TBX1 expresses progenitors involved with the development of the right ventricle.
Uridine 5-diphospho-glucuronosyltransferase (UDP-glucuronosyltransferase, UGT) is a microsomal glycosyltransferase (EC 2.4.1.17) that catalyzes the transfer of the glucuronic acid component of UDP-glucuronic acid to a small hydrophobic molecule. This is a glucuronidation reaction.Alternative names:

glucuronyltransferase
UDP-glucuronyl transferase
UDP-GT

Function
Glucuronosyltransferases are responsible for the process of glucuronidation, a major part of phase II metabolism. Arguably the most important of the Phase II (conjugative) enzymes, UGTs have been the subject of increasing scientific inquiry since the mid-to-late 1990s. The reaction catalyzed by the UGT enzyme involves the addition of a glucuronic acid moiety to xenobiotics and is the most important pathway for the human bodys elimination of the most frequently prescribed drugs. It is also the major pathway for foreign chemical (dietary, environmental, pharmaceutical) removal  for most drugs, dietary substances, toxins and endogenous substances. UGT is present in humans, other animals, plants, and bacteria. Famously, UGT enzymes are not present in the genus Felis, and this accounts for a number of unusual toxicities in the cat family. The glucuronidation reaction consists of the transfer of the glucuronosyl group from uridine 5-diphospho-glucuronic acid (UDPGA) to substrate molecules that contain oxygen, nitrogen, sulfur or carboxyl functional groups. The resulting glucuronide is more polar (e.g. hydrophilic) and more easily excreted than the substrate molecule. The product solubility in blood is increased allowing it to be eliminated from the body by the kidneys. Diseases
A deficiency in the bilirubin specific form of glucuronosyltransferase is thought to be the cause of Gilberts syndrome, which is characterized by unconjugated hyperbilirubinemia.