Chromosome 22q11 deletions also deleting TBX1 gene have been seen in 17% TOF cases. FLT4 gene expression leads to Vascular endothelial growth factor receptor 3 (VEGFR-3) which helps vascularization. Mutations of this gene have been associated with TOF, accounting for 2.4% of all cases. FOXC2 is another gene involved in embryonic development of the cardiac system. Mutations of this gene have been shown to result in dysfunctional lymphatic syndrome and TOF. GATA4 aids in cardiac development by helping increase the production of cardiomyocytes. Mutations of this gene have been seen in various familial TOF cases often lasting 2-3 generations. FLNA is a protein coded by the gene of the same name that crosslinks actin filaments into networks in cytoplasm and helps anchor membrane proteins for the actin cytoskeleton. Mutations of this gene were seen to cause TOF in some patients.The Environmental Factors that have been studied to potentially be associated TOF include:

Maternal Alcohol consumption: During embryonic development, many of the body’s processing and filtration systems are not fully developed. Fetal body is unable to process alcohol as well as adults which can lead to improper development, including cardiogenesis. While no conclusive evidence has been found between effects of alcohol consumption and TOF, maternal alcohol consumption has been seen in various patients with TOF. Maternal smoking: Maternal smoking has been associated with various fetal complications such as premature delivery and low birth weight which can lead to TOF.
See also
Trilogy of Fallot
Congenital rubella syndrome

References
External links

What Is Tetralogy of Fallot? at the National Institutes of Health
Understanding your childs heart: Tetralogy of Fallot by the British Heart Foundation