Although cardiac fibroblast-derived EVs play a critical role in inducing cardiac hypertrophy by activating the renin-angiotensin system in cardiomyocytes [121], the EV-enriched miRNAs secreted by cardiac fibroblasts in response to cardiac stress, such as miRNA-21-3p [41] and miRNA-27a-5p [42], can also be taken up by cardiomyocytes, resulting in the cardiac hypertrophy via translational inhibition of both SORBS2 and PDLIM5 [41] or PDLIM5 [42]. The gene discussed is PDLIM5; the disease is cardiac hypertrophy.