The ACVR2A (Activin A Receptor Type 2A) gene encodes a transmembrane serine-threonine kinase receptor that functions as a Type II receptor in the Transforming Growth Factor-beta (TGF-beta) superfamily signaling pathway. The encoded protein is primarily involved in ligand-binding (e.g., activins A and B, inhibin A, and specific bone morphogenetic proteins like BMP-7), forming heterodimeric complexes with Type I receptors to initiate downstream signaling cascades, often involving SMAD transcription factors, which regulate cell growth, differentiation, and apoptosis ^[1]. Gene expression is observed in numerous tissues, including high levels in the placenta, endometrium, testes, prostate, ovary, skeletal muscle, heart, and neural tissues such as the hypothalamus and cerebral cortex, underscoring its diverse biological roles. Dysfunction or polymorphisms in ACVR2A have been implicated in several diseases, notably preeclampsia (a severe pregnancy disorder associated with decreased placental ACVR2A expression and impaired trophoblast invasion) and various cancers, particularly colorectal and gastric cancers with microsatellite instability, where loss of receptor expression contributes to tumor pathogenesis ^[2-3].

B6-huACVR2A mouse is a humanized model generated using gene editing technology, in which the sequences from the ATG start codon to partial 3’UTR (downstream of mouse Orc4 3’UTR) of mouse Acvr2a gene are replaced with the sequences from ATG start codon to downstream of 3’UTR of human ACVR2A gene. This model can be used for research related to malignant tumors such as colorectal cancer and gastric cancer, bone and cartilage development diseases, reproductive system and gonad development, as well as the development of ACVR2A-targeted drugs.