Our results revealed that a 2 M administration of a subpressor dose of Ang II without pressure overload could induce late cardiomyopathy at 4 M and 6 M, as demonstrated by a progressive increase in cardiac remodeling (elevated LVID and LVPW) and dysfunction (decreased EF and FS values), following a significant increase in cardiac NLRP3 inflammasome activation (indicators of NLRP3, caspase-1 and IL-1β) and oxidative damage (indicators of 3-NT and 4-HNE) (Figure 1 and Figure 2). This evidence concerns the gene AGT and cardiomyopathy.