We read the comments offered by Wang et al on our recent publication on the cardiovascular preventing pleiotropic effects of dipeptidyl peptidase–4 (DPP-4) inhibitors. Most of the comments provided by Wang et al are included in our report, including the myocardial homing effects of endothelial progenitor cells by the stromal-derived factor–1α/C-X-C chemokine receptor type 4 axis and the myocardial regenerating effects of the granulocyte-colony stimulating factor. The difference is that in our review, we stress that the cardiovascular preventing pleiotropic actions of DPP-4 inhibitors are mediated, mainly, through the incretin glucagon-like peptide–1. In their elegant and detailed study, Yin et al attempted to show that the DPP-4 inhibitor vildagliptin exerted its beneficial remodeling effects in post–myocardial infarction nondiabetic rats, independently of glucagon-like peptide–1. However, reading through their report, there is a trend for decreased post–myocardial infarction scarring in rats treated with vildagliptin compared with myocardial infarction placebo, although not statistically significant. In addition, in their discussion, the investigators discuss the possible implications of glucagon-like peptide–1 in the beneficial antiremodeling effects in their post–myocardial infarction rat model. Also, their results are at variance with those of other similar studies and need to be confirmed by future studies. In addition, they used nondiabetic rats, and this could be the difference in their results. Finally, our review was concise and limited by word count and reference number imposed by the journal, and we reached both limits. Also, vildagliptin is not approved for use in the United States, and most likely it will not be, and the interest in this subject is limited. In conclusion, this is a fast evolving field, and future studies will hopefully provide additional information regarding the cardiovascular effects of DPP-4 inhibitors.