In conclusion, we uncovered a novel proangiogenic role of FMO2 through the metabolic regulation of N‐acetylornithine by transcriptionally inhibiting the ATF3‐NOTCH1 pathway (Figure 7W), highlighting the translational relevance of FMO2 and its metabolite N‐acetylornithine as novel therapeutic targets for treating ischemic diseases. This evidence concerns the gene ATF3 and ischemic disease.