Kirrel2, a member of the immunoglobulin superfamily, is also known as kin of irregular chiasm-like 2. It contains five Ig domains, a transmembrane domain, and an intracellular domain. Kirrel2 is involved in multiple biological processes. In the olfactory system, it may regulate the targeting of axons in the olfactory bulb; in pancreatic β -cells, it is associated with the regulation of basal insulin secretion; and it may also play a role in the development of the cerebellum and in the function of perivascular astrocyte endfeet in the brain [3,4,5,6].

In mice lacking Kirrel2, MOR174-9-and M72-expressing olfactory sensory neuron (OSN) axons, which project to the DII region of the olfactory bulb, target ectopic glomeruli, indicating that Kirrel2 is required for axonal coalescence in subsets of OSNs projecting to this region [1]. In Group 3 medulloblastomas, high expression of KIRREL2 is an independent molecular prognostic indicator of poor patient survival, and integrating its expression in risk-stratification models may improve outcome prediction for this tumor type [2]. In pancreatic β -cells, Kirrel2 knockdown or genetic deletion in mice leads to increased basal insulin secretion, suggesting its role in regulating insulin release [5].

In conclusion, Kirrel2 is essential for axonal targeting in specific OSN populations in the olfactory bulb, prognosis prediction in Group 3 medulloblastomas, and the regulation of basal insulin secretion in pancreatic β -cells. The study of Kirrel2 using gene-knockout mouse models has provided valuable insights into these biological processes and disease-related mechanisms, which may contribute to better understanding of related diseases and potentially guide the development of new therapeutic strategies.