Tumor-Associated Calcium Signal Transducer 2, encoded by the TACSTD2 gene, is a prominent type I transmembrane glycoprotein critically involved in mediating diverse cellular processes ^[1]. Acting primarily as a cell surface receptor, TROP2 transduces extracellular signals to initiate intracellular calcium release, thereby influencing key cellular behaviors including proliferation, adhesion, migration, and differentiation. While its expression is notably high during embryonic development, particularly in fetal tissues and trophoblasts, and maintained at lower levels in some normal adult epithelial lineages, aberrant and significant upregulation of TROP2 is a hallmark feature across a wide spectrum of human carcinomas ^[2]. This dysregulated expression contributes substantially to tumor initiation, progression, and metastasis by modulating various signaling pathways ^[3]. Beyond its role in oncogenesis, germline mutations in TACSTD2 are identified as the underlying cause of the rare autosomal recessive disorder, gelatinous drop-like corneal dystrophy ^[4]. The distinct expression profile of TROP2, with its high levels in numerous solid tumors contrasted by limited expression in most healthy adult tissues, positions it as a compelling and clinically relevant target for developing targeted therapies, notably antibody-drug conjugates, aimed at treating TROP2-expressing cancers ^[3].

The B6-hTROP2 (hTACSTD2) mouse is a humanized model constructed by replacing the signal peptide and extracellular domain of the mouse Tacstd2 with the corresponding signal peptide and extracellular domain from the human TACSTD2 gene. The B6-hTROP2 (hTACSTD2) mice can be used for studies on pathogenesis of various cancers, as well as for TACSTD2-targeted drug development.