Thy1, also known as CD90, is a heavily N-glycosylated, glycophosphatidylinositol (GPI) anchored cell surface protein. It plays diverse roles in various biological processes. It has been associated with pathways such as the regulation of adipogenesis, epithelial-mesenchymal transition (EMT), and adherens junction formation. Its dysregulation is related to diseases including cancer, obesity, and glomerulonephritis [1-4, 7-10]. Gene knockout (KO) mouse models can be valuable for studying its functions.

In the epidermis, Thy1 marks a distinct population of slow-cycling stem cells. Ablation of Thy1+ cells strongly impairs epidermal replenishment and wound repair, indicating their non-redundant function in epidermal homeostasis and repair [1]. In adipogenesis, DNA methylation regulates Thy1 expression, and Thy1-knockout mice are prone to diet-induced obesity [2]. In nasopharyngeal carcinoma, THY1 functions as a tumor suppressor, and its down-regulation is associated with tumor metastasis. Knockdown of THY1 disrupts adherens junctions and increases tumor invasion [3].

In conclusion, Thy1 has essential functions in epidermal maintenance, adipogenesis regulation, and tumor suppression. Studies using KO mouse models have revealed its significance in epidermal homeostasis, obesity-related processes, and cancer metastasis. These findings contribute to our understanding of the role of Thy1 in these specific disease areas.