Fig. 1

Since the opening of the first gene STK39 [fig 1, fig. 2](function: may act as a mediator of stress-activated signals. This gene encodes a serine/threonine kinase that is thought to function in the cellular stress response pathway. The kinase is activated in response to hypotonic stress, leading to phosphorylation of several cation-chloride-coupled cotransporters. The catalytically active kinase specifically activates the p38 MAP kinase pathway, and its interaction with p38 decreases upon cellular stress, suggesting that this kinase may serve as an intermediate in the response to cellular stress) in the field of genetics, which is responsible for activating the pressure rise was not much time, and the scientific community had almost come to an understanding of the essence of this complex process. From the very beginning of genetic research in this direction was assumed that the STK39 gene is just the tip of the iceberg and that there are still many studies before we can draw at least some concept of genetic regulation of blood pressure. One of the last three modern research in this field, shed light on this perspective was provided by article ”Genome-wide association study identifies eight loci associated with blood pressure” Nature Genetics (June 2009, Volume 41) which contains the test results for 2,5 million genotyped for the relationship of systolic and diastolic blood pressure by genotype (European, Asian, Indian).

Fig.2

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