FoxF2 is a transcriptional factor that initiates gene expression. Foxf2 is particularly expressed in central nervous system pericytes. Recent studies have displayed that an inactivation of Foxf2 in mice had an impact on the blood-brain barrier integrity with evidence of breakdown. During angiogenesis, the protein pdgf-B is synthesized by endothelial cells and is detected by pdgfr-𝛽 expressed on pericytes. Fibrinogen is a glycoprotein that participates in coagulation. It is undetectable in a healthy brain due to an intact barrier, making it an important biomarker in neurological diseases. Pericytes are a part of the microvascular unit and are wrapped around endothelial cells, which make up the blood-brain barrier. Pericytes play an important role in bloodvessel formation, development of vessel stability, regulation of blood flow, and the integrity and formation of vascular barrier. The aim of this study was to induce a pericyte specific knockout mutation of Foxf2 and investigate possible fibrinogen extravasation in the brain and pdgfr-𝛽 expression. Using Cre/loxP recombination mouse knockouts were created in vivo by Tamoxifen injections and the . Immunohistochemistry was performed to investigate fibrinogen and pdgfr-𝛽 expression. Pdgfr-𝛽 expression was further validated with RT-qPCR on an in vitro induced cell culture. Immunohistochemistry slides suggested that the knock-out mutation of Foxf2 caused a disrupted blood-brain barrier resulting in extravasated fibrinogen. However, immunohistochemistry images confirmed with RT-qPCR on pdgfr-𝛽 expression displayed no distinct difference. Due to a small sample size, RT-qPCR needs more validation and since immunohistochemistry only allows for interpretation, further study is required.