Traditionally, research and medical practice focus on reducing cardiovascular disease risk by acting on diet and lifestyle during a patient’s adult life, while considering transgenerational risk only in the relatively few clear cases of genetic predisposition. A complementary view to that one is gaining ground, as it is clear that cardiovascular risk (CVR) can be transmitted from mother to progeny and across progeny generations in a way that is distinct from mere inheritance of genetic variants. Extensive reviews have discussed the conceptual framework and experimental evidence for these phenomena in cardiovascular disease (CVD) and other conditions [2,3]. Changes in epigenetic marks are likely to explain a number of cases of nongenetic transmission of CVR. Epigenetics provides a model of transcriptional regulation that can be at the same time mitotically/meiotically stable and flexible enough to respond to dietary and environmental factors, thus explaining how these latter can modify the existing gene expression pattern into a new and, crucially, stable and self-sustaining one . Borrowing from the well established concept of metabolic programming, that is resetting of the existing biochemical machinery by a transient stimulus to produce a new, stable cellular phenotype [1,5], those phenomena are collectively regarded as examples of ‘epigenetic programming’.