Mdfic, encoding the MyoD family inhibitor domain containing protein, is involved in multiple biological processes. It functions as a transcriptional regulator and is associated with pathways related to cell migration, myogenic differentiation, and immune response [1,2,4]. Its importance lies in its roles in lymphatic vasculature development, myoblast proliferation, differentiation and apoptosis, as well as in some cancer-related processes [1,2,3]. Genetic models, especially mouse models, are valuable for studying Mdfic's functions.

In a mouse model of human MDFIC truncation variants, homozygous mutant mice died perinatally with chylothorax, and their lymphatic vasculature was mispatterned with major defects in lymphatic vessel valve development. Mechanistically, MDFIC controls collective cell migration during lymphatic vessel valve formation by regulating integrin β1 activation [1]. In chicken myoblasts, miR-146b-3p inhibits MDFIC, suppressing myoblast proliferation and differentiation and promoting apoptosis [2]. In fetal bovine skeletal muscle-derived progenitor cells, knockdown of MDFIC facilitated myogenic differentiation [4].

In conclusion, Mdfic is crucial for lymphatic vasculature development, myogenic processes, and may have implications in cancer and immune-related diseases. Mouse models of Mdfic truncation variants have revealed its role in lymphatic vessel development, highlighting its importance in understanding lymphatic diseases [1].