Moreover, it is intriguing to consider the established role of A-to-I editing in control of angiogenesis—a key process in HF190,304,305—via editing of miRNAs65, 66, 67 jointly with miR-1, which has been implicated in cardiogenesis,296 hypertrophy,297, 298, 299,306 cardioprotection,307 and atherosclerosis,308 as it represses ADAR1 non-cardiac tissues300,301 and acts oppositely in favor of hypertrophy when modified by oxidation.302. This evidence concerns the gene ADAR and atherosclerosis.