MFng, also known as Manic Fringe, is a member of the Fringe family of β1,3-N-acetylglucosaminyltransferases. It modulates Notch signaling, which is crucial in various biological processes such as cell differentiation, development, and disease [3,7].

In cancer research, MFng has shown significance. In osteosarcoma, its high expression is an independent adverse prognostic factor for disease-free survival, promoting cell proliferation and inhibiting apoptosis in U2OS cells [1]. In triple-negative breast cancer, it activates the Notch signaling and promotes cancer progression, while the GATA3/miR205-5p axis can inhibit its transcription [2]. In renal cell carcinoma, it is up-regulated, and its down-regulation in endothelial cells impedes angiogenesis and cancer cell migration [4,5].

In heart development, MFng promotes endothelial-to-mesenchymal transition (EndMT) mediated by the Notch signaling pathway during heart valve development, and a deleterious MFng mutation was found in patients with tetralogy of Fallot-pulmonary valve stenosis (TOF-PS) [6]. It also plays a role in ventricular chamber development, with its early endocardial expression promoting Dll4-Notch1 signaling for trabeculation, and its down-regulation required for ventricular maturation [8].

In conclusion, MFng is essential in modulating Notch signaling, influencing multiple biological processes. Its role in cancer prognosis and progression, as well as in heart development and associated diseases, makes it an important gene for further research. Studies on MFng using genetic models contribute to understanding disease mechanisms, potentially leading to new diagnostic and therapeutic strategies.