Ntn1, also known as Netrin-1, is a gene that plays diverse and significant roles in various biological processes. It is involved in processes such as axon guidance, cell migration, and angiogenesis. In the context of signaling pathways, it can interact with multiple receptors like UNC5B to regulate different cellular responses, and is important for normal development and tissue homeostasis [4,5].

In porcine studies, NTN1-CNV affects intramuscular fat (IMF) content. Knock-down and over-expression experiments in C2C12 cells showed that NTN1 influences the proliferation and differentiation of muscle cells, potentially via the AMP-activated protein kinase (AMPK) pathway [1]. In cancer research, netrin-1 blockade using an anti-netrin-1 antibody (NP137) inhibits tumour growth and epithelial-to-mesenchymal transition (EMT) in endometrial cancer and skin squamous cell carcinoma (SCC) [2,3]. In mouse models of peripheral nerve injury, NTN1-high endothelial cells and their exosomes are critical for the formation of the vascular niche, promoting nerve repair [4]. In atherosclerotic mouse models, silencing myeloid Ntn1 reduces plaque burden and promotes inflammation resolution [6].

In conclusion, Ntn1 is essential for multiple biological processes including muscle development, tumour progression, nerve repair, and atherosclerosis. Gene-knockout or conditional-knockout mouse models, along with in vitro cell-based experiments, have been crucial in uncovering these functions. Understanding Ntn1's role provides potential therapeutic targets for various diseases such as cancer, nerve injury, and atherosclerosis.