Wnt proteins are extracellular [[growth factor]]s that activate intracellular signalling pathways. There are two types of pathways: canonical and non-canonical. The classic canonical Wnt pathway involves [[Beta-catenin|Bβ-catenin]] protein as a signaling mediator. Wnt maintains Bβ-catenin by preventing against [[Proteasome]] degradation. Thus, Bβ-catenin is stabilized in the presence of Wnt and regulates gene transcription through interaction with TCF/LEF transcription factors.<ref name="Gessert (2010)">Gessert S. and Kuhl M. [http://circres.ahajournals.org/content/107/2/186.full "The multiple phases and faces of wnt signaling during cardiac differentiation and development."] Circulation Research, 2010 107(2) p 186 - 199 {{doi|10.1161/CIRCRESAHA.110.221531}}. Accessed 19 November 2012.</ref> The canonical Wnt/Bβ-catenin pathway is important for control of cell proliferation.<ref name="Kirby (2010)2">Kirby M. L. and Hutson M. R. [https://dx.doi.org/10.4161/cam.4.4.13489 "Factors controlling cardiac neural crest cell migration."] Cell adhesion and migration, December 2010 4(4). Accessed 20 November 2012.</ref> The non-canonical Wnt pathway is independent of Bβ-catenin and has an inhibitory effect on canonical Wnt signaling.<ref name="Gessert (2010)"/>
Wnt signaling pathways play a role in CNCC development as well as OFT development.<ref name="Gessert (2010)"/> In mice, decrease of Bβ-catenin results in a decrease in the proliferation of CNCCs.<ref name="Gessert (2010)"/> Downregulation of the Wnt coreceptor Lrp6 leads to a reduction of CNCCs in the dorsal neural tube and in the pharyngeal arches, and results in ventricular, septal, and OFT defects.<ref name="Gessert (2010)"/> Canonical Wnt signaling is especially important for cell cycle regulation of CNCC development and the initiation of CNCC migration.<ref name="Gessert (2010)"/> Non-canonical Wnt signaling plays a greater role in promoting cardiac differentiation and OFT development.<ref name="Gessert (2010)"/>
