Snai3, a member of the Snail gene family, encodes a zinc finger-containing transcriptional repressor protein. It is involved in regulating cell-lineage determination in the hematopoietic system, and may play roles in processes like folliculogenesis, luteinization, and early embryonic development [1,3]. In the hematopoietic system, it can influence the development of lymphoid and myeloid lineages. In ovarian and embryonic processes, its expression pattern suggests potential regulatory functions [1,3]. Genetic mouse models are valuable for studying Snai3's functions.

In gene knockout studies, Snai3 null mutant homozygous mice are viable and fertile, indicating that Snai3 is not essential for embryogenesis [4]. Deletion of both Snai2 and Snai3 in mice leads to impaired physical development, lymphocyte deficiency, and stunted growth, suggesting some functional redundancy or cooperation between Snai2 and Snai3 [2]. Also, Snai3 does not have a major role in regulating skeletal muscle regeneration in mice [5].

In conclusion, Snai3 is not essential for embryogenesis or skeletal muscle regeneration in mice. However, its combined deletion with Snai2 impairs physical and immune cell development. These gene knockout mouse models have provided insights into Snai3's role in development and immune-related processes, helping to understand its biological functions and potential implications in related diseases.