**5. Summary**

In the past decade, there has been increasing evidence from both experimental and human studies that KLF15 is an important regulator of cardiac hypertrophy. The studies clearly support a pathological role of KLF15 in the development of cardiac hypertrophy and identify KLF15 as part of a transcriptional pathway regulating the cardiac response to hypertrophic stimuli. Thus, loss of KLF15 leads to transcription repression and stimulates fibrotic signaling pathways. Overexpression studies suggest KLF15 inhibits hypertrophy and reduces cardiomyocyte size and pro-hypertrophic and pro-fibrotic markers such as ANP, BNP and CTGF. Genetic variants in *KLF15* may also contribute to the development of LVH and predict heart failure outcomes in those with LVH. The genetic findings complement the human studies which reported reduced KLF15 expression in the hearts of patients with LVH and heart failure. The only suggested therapeutic pathway for preventing loss of KLF15 and transition to heart failure thus far has been inhibition of the p53 and p300 pathway.

**Conflicts of Interest:** The authors declare no conflict of interest.
