Hao reported that YAP can regulate multiple genes including BIRC5, ITGB2, IGFBP3 and p57 to promote survival and migration of MCF10A cells. Interestingly, we did not detect any of these genes except BIRC5 in our HUVEC study, a discrepancy that may be the result of tissue-specific differences in YAP transcriptional outputs, since none of the aforementioned studies utilized HUVEC cells. Another reason that we identified a different set of YAP targets compared to other gene knockdown studies may involve differences in experimental design. Our study used an early time-point in order to preferentially identify proximal targets, as opposed to other studies which examined cells between 48 h and 5 d after YAP knockdown. Irrespective of these differences, the list of candidate genes we observed is most consistent with the one reported by Kapoor et al., which concluded that YAP cooperates with E2F1 in Kras LEE011 induced pancreatic adenocarcinoma by modulating a large subset of E2F1 targets including Cdc6, Cdk1, Mcm complex components and Rad51. Taken together with the results of Kapoor et al., our study suggests that YAP regulates HUVEC cell proliferation via a specific set of E2F1 regulated cell cycle determinants. Human epidemiological studies as well as a variety of animal ones revealed that prenatal and early postnatal nutritional statuses may influence adult susceptibility to impaired glucose tolerance, cardiovascular disease, and obesity. However, little is known about the mechanism underlying these phenomena. While increasing evidence suggests thatmaternal fatty acid status during pregnancy and lactation greatly influences newborn and infant health, very few studies have paid attention to the long-term consequences of changing the maternal dietary fatty acid composition. Different dietary fatty acids modulate different biologically-relevant pathways. As an example, a recent study in rats demonstrated that the intake of high amounts of n-3 fatty acids compared to other types of fatty acids during early pregnancy reduces fat accretion and age-related decline in insulin sensitivity in male offspring. However, the precise nature of these effects remains elusive. In addition to diet, epigenetic modifications may influence gene expression and modulate the phenotype of the organism much later in life, via exposure to an altered intra-uterine milieu or metabolic perturbation. MicroRNAs are small endogenous non-coding RNAs that regulate several cellular and biologic processes by regulating gene expression. By targeting complex biological AZ 960 pathway, miRNAs ��fine-tune�� gene expression under physiologic conditions, but it is under conditions of stress when their function becomes especially pronounced, underscoring their role in health and disease.