The TGFB2 gene encodes transforming growth factor-beta 2 (TGF-β2), a secreted multifunctional cytokine that regulates cell proliferation, differentiation, apoptosis, and extracellular matrix production ^[1]. It is expressed in various tissues, including epithelial cells, mesenchymal cells, immune cells, and neural tissues, playing critical roles in embryonic development, immune regulation, and tissue homeostasis. The encoded protein is synthesized as an inactive precursor that undergoes proteolytic cleavage to release the active TGF-β2 ligand, which signals through SMAD-dependent and SMAD-independent pathways ^[1]. Dysregulation of TGFB2 is linked to cardiovascular diseases (e.g., Marfan syndrome, aortic aneurysms), fibrosis, cancer (both tumor-suppressive and pro-metastatic roles), and developmental disorders (e.g., Loeys-Dietz syndrome) ^[2-3]. Additionally, TGFB2 mutations or aberrant expression can contribute to ocular defects, craniofacial abnormalities, and immune dysregulation ^[4]. Its pleiotropic effects make it essential in both normal physiology and disease pathogenesis.

The B6-hTGFB2 mouse is a humanized model, constructed by replacing the partial coding sequences of mouse Tgfb2 exon 1 with the Kozak-Human TGFB2 CDS-3’UTR of the Human TGFB2-WPRE-BGH pA cassette. B6-hTGFB2 mice can be used for research into the pathogenesis of cardiovascular diseases, fibrosis, cancers, and developmental disorders. They are also useful for the screening, development, and safety evaluation of TGFB2-targeted drugs.