Although the hepatic presentation was assumed to mean more severely deranged ATP7B function, modifier genes, such as the 5,10-methylenetetrahydrofolate reductase gene, environmental factors, such as nutritional copper intake, infectious disease, drug and toxin, and other epigenetic factors must be at play in the overall phenotypic expression of WD in individuals [15], [16]. Here, ATP7B is linked to infectious disease.