This might have led to an underestimation of the impairment in physical QoL and its relation with cardiovascular disease severity. The main limitation of this study is a relatively small sample size. The highest p-value in the genetic association study did not reach the targeted p-value after Bonferroni correction. Most SNPs in the IL4R gene had p-values less than 0.05 which suggest the association is not likely to be incidental. As these associations do not seem to be MFS specific, validation in patients with different pathology or even in a healthy population could yield interesting results. This is still the largest study on QoL in MFS patients and the first study exploring the genetic basis of their QoL. In conclusion, we found a genetic basis for mental QoL in cytokine genes and their activity. This relation does not seem specific for MFS and is independent of patient characteristics. Knowledge about this genetic component of QoL provides insight and can eventually allow us to identify patients susceptible to poor QoL. This information might guide clinicians in deciding making, opting for treatments with the smallest negative impact on QoL. Furthermore, we will be able to better target specific support to those who need it. Note that validation in larger patient populations is warranted. Ultimately, immuno logical treatment strategies can be developed to improve patients’ QoL. Stroke is currently the third leading cause of death in western societies. To reduce the impact on society, one must Reversine either reduce the number of strokes, the severity of the stroke or improve recovery from stroke. This paper relates to reduction of the severity of the stroke once it occurs. Since a stroke is an ischemic event, the tissue is starved of nutrients including oxygen, which leads to hypoxia. Many species are hypoxia tolerant, and so it is reasonable to consider whether the broad spectrum of transcriptional changes that occur on exposure to hypoxia could induce adaptive protection against hypoxic/ischemic damage in the human brain. When exposed to hypoxia, there is an increase in hypoxia inducible factor content and a host of “downstream” genetic events which serve to improve the capacity of the tissue to survive low oxygen conditions. Hypoxia acclimation includes increased capacity to supply oxygen, remove end-products and produce energy from anaerobic means. These events include an increase in hematocrit, vascular density, glycolytic capacity and glycogen content. We use the term acclimation for the changes which would occur within the lifetime of an animal because in the comparative physiology literature the term adaptation refers to changes to the species over generations.Which involve hypoxia and ischemia. Should this be validated, then it opens avenues for potential improvement of stroke outcome. One potential avenue for improving outcome which may be similar in mechanism would be to upregulate HIF-1a. Stabilization of HIF-1a allows HIF to dimerize and to stimulate the hypoxia response genes. There is a significant literature on hypoxic/ischemic preconditioning. A range of mechanisms are proposed in preconditioning which could impact stroke severity including, but not limited to, a reduction of inflammation, histamine regulation, endothelial reactivity, reactive oxygen species, increased vascular endothelial growth factor and increased erythropoietin. Cell culture studies indicate that preconditioning can occur through intracellular genetic modifications.