Extracellular vesicles derived from trophoblastic stem cells (TSCs) could transfer miRlet-7i to myocardial cells, inhibit the inflammatory response, and reduce myocardial cell apoptosis and fibrosis by downregulating YAP1 activity, accompanied by a decrease in the expression levels of the YAP target genes ctgf and TEAD. Thus, DOX-induced myocardial remodeling and heart failure can ultimately be reversed, thereby improving dilated cardiomyopathy and cardiac dysfunction caused by doxorubicin treatment (Ni et al., 2020). The gene discussed is YAP1; the disease is dilated cardiomyopathy.