For example, little is known today regarding the contribution to cardiovascular disease onset of other somatic mutations recognized in MPN subjects, i.e., mutations in the calreticulin (CALR) or myeloproliferative leukemia protein (MPL) driver genes, or about the interplay between HTN and genetic alterations in epigenetic regulators, e.g., DNA methyltransferase 3 alpha (DNMT3A), tet methylcytosine dioxygenase 2 (TET2), additional sex comb-like transcriptional regulator 1 (ASXL1), isocitrate dehydrogenase 1 or 2 (IDH1/2) genes [14,15,99,100]. The gene discussed is MPL; the disease is cardiovascular disorder.