be caused by epigenetic changes (or "epimutations") on both the alleles, rather than involving any genetic mutation. In all 19 informative cases, the epimutations that, together with physiological imprinting and therefore silencing of the other allele, were causing these syndromes were localized on a chromosome with a specific parental and grandparental origin. Specifically, the paternally derived chromosome carried an abnormal maternal mark at the SNURF-SNRPN, and this abnormal mark was inherited from the paternal grandmother. Similarly, epimutations on the MLH1 gene has been found in two individuals with a phenotype of hereditary nonpolyposis colorectal cancer, and without any frank MLH1 mutation which otherwise causes the disease. The same epimutations were also found on the spermatozoa of one of the individuals, indicating the potential to be transmitted to offspring. In addition to epimutations to the MLH1 gene, it has been determined that certain cancers, such as breast cancer, can originate during the fetal stages within the uterus. Furthermore, evidence collected in various studies utilizing model systems (i.e. animals) have found that exposure during parental generations can result in multigenerational and transgenerational inheritance of breast cancer. More recently, studies have discovered a connection between the adaptation of male germinal cells via pre-conception paternal diets and the regulation of breast cancer in developing offspring. More specifically, studies have begun to uncover new data that underscores a relationship between transgenerational epigenetic inheritance of breast cancer and ancestral alimentary components or associated markers, such as birth weight. By utilizing model systems, such as mice, studies have shown that stimulated paternal obesity at the time of conception can epigenetically alter the paternal germ-line. The paternal germ-line is responsible for regulating their daughters’ weight at birth and the potential for their daughter to develop breast cancer. Furthermore, it was found that modifications to the miRNA expression profile of the male germline is coupled with elevated body weight. Additionally, paternal obesity resulted in an increase in the percentage of female offspring developing carcinogen-induced mammary tumors, which is caused by changes to mammary miRNA expression. Aside from cancer related afflictions associated with the effects of transgenerational epigenetic inheritance, transgenerational epigenetic inheritance has recently been implicated in the progression of pulmonary arterial hypertension (PAH). Recent studies have found that transgenerational epigenetic inheritance is likely to be involved in the progression of PAH because current therapies for PAH do not repair the irregular phenotypes associated with this disease. Current treatments for