The expression of inflammatory genes can also be triggered by activated CaMKII in cardiomyocytes in the mice TAC model, while by knocking out CaMKIIδ, inhibiting monocyte chemotactic protein-1 (MCP-1), and suppressing inflammasome are able to effectively reverse cardiac remodeling (Suetomi et al., 2018; Suetomi et al., 2019). The gene discussed is CCL2; the disease is persistent truncus arteriosus.