CDH13, also known as T-cadherin or H-cadherin, is an atypical member of the cadherin family. It is a cell adhesion molecule anchored to the cell surface membrane via a glycosyl phosphatidyl inositol (GPI) moiety. CDH13 has been implicated in various biological processes, including axonal growth cone development, synapse morphogenesis, and embryonic neural tube formation. It may also be involved in regulating lipid metabolism during adipogenesis [3,4,5,6,7].

In a CDH13-deficient mouse model, early-life stress led to increased anxiety-like behavior compared to other genotypes, indicating a role of CDH13 in the programming of and adaptation to early-life stress [4]. In chronic myeloid leukemia (CML) cells, activation of CDH13 expression by small RNA promoted cell apoptosis by inhibiting the NF-κB signaling pathway, overcoming BCR-ABL1-independent resistance to imatinib [2]. In clear cell renal cell carcinoma (ccRCC), CDH13 was significantly upregulated and strongly correlated with better survival, lower cancer stages, and lower tumor grades [1].

In conclusion, CDH13 plays important roles in neurodevelopment, adipocyte differentiation, and cancer-related processes. Gene knockout mouse models have been crucial in revealing its functions in early-life stress adaptation, CML drug resistance, and ccRCC prognosis, providing insights into potential therapeutic targets and disease mechanisms.