PAH have attempted to correct symptoms of PAH with vasodilators and antithrombotic protectors, but neither has effectively alleviated the complications related to the impaired phenotypes associated with PAH. The inability of vasodilators and antithrombotic protectants to correct PAH suggests that the progression of PAH is dependent upon multiple variables, which is likely to be consequent of transgenerational epigenetic inheritance. Specifically, it is thought that transgenerational epigenetics is linked to the phenotypic changes associated with vascular remodeling. For example, hypoxia during gestation may induce transgenerational epigenetic alterations that could prove to be detrimental during the early phases of fetal development and increase the possibility of developing PAH as an adult. Taking the potential effects of transgenerational epigenetics during fetal development into consideration is derived from the fetal origins of adult disease (FOAD) hypothesis, which is related to the concept of fetal programming. Though hypoxic states could induce the transgenerational epigenetic variance associated with PAH, there is strong evidence to support that a variety of maternal risk factors are linked to the eventual progression of PAH. Such maternal risk factors linked to late-onset PAH includes placental dysfunction, hypertension, obesity, and preeclampsia. These maternal risk factors and environmental stressors coupled with transgenerational epigenetic changes can result in prolonged insult to the signaling pathways associated with the vascular development during fetal stages, thus increasing the likelihood of having PAH. One study has shown childhood abuse, which is defined as "sexual contact, severe physical abuse and/or severe neglect," leads to epigenetic modifications of glucocorticoid receptor expression. Glucocorticoid receptor expression plays a vital role in hypothalamic-pituitary-adrenal (HPA) activity. Additionally, animal experiments have shown that epigenetic changes can depend on mother-infant interactions after birth. Furthermore, a recent study investigating the correlations between maternal stress in pregnancy and methylation in teenagers/their mothers has found that children of women who were abused during pregnancy were more likely to have methylated glucocorticoid-receptor genes. Thus, children with methylated glucocorticoid-receptor genes experience an altered response to stress, ultimately leading to a higher susceptibility of experiencing anxiety. Additional studies examining the effects of diethylstilbestrol (DES), which is an endocrine disruptor, have found that the grandchildren (third-generation) of women exposed to DES significantly increased the probability of their grandchildren developing attention-deficit/hyperactivity disorder (ADHD). This is because women exposed to endocrine disruptors, such as DES, during gestation may be linked to multigenerational neurodevelopmental deficits. Furthermore, animal studies indicate that endocrine disruptors have a profound impact