The possible trigger mechanisms of combined PE are linked to the processes that are carried out by the products of the identified genes, namely, inflammation (IL1B), endothelial dysfunction (NOS3), heat shock and stress (HSPA4), stabilizing cell membranes at diverse fluid-tissue interfaces and protecting the vascular endothelium from an attack by some factors in plasma, such as active complement complexes (CLU), and homocysteine metabolism (MTHFR). This evidence concerns the gene HSPA4 and endothelial dysfunction.