Dr. Packer recently proposed an intriguing hypothesis that DPP-4 inhibitors potentiate some endogenous peptides, such as stromal cell-derived factor-1, in addition to activation of GLP-1, and that unfavorable effects of those peptides on CV parameters (e.g., inflammation, fibrosis, plaque growth, and sympathetic activation) could prevail against the CV protective effects of GLP-1, possibly leading to worsened CV complications and HF [36, 37]. Here, GLP1R is linked to hydrops fetalis.