[5] Through lineage tracing and timelapse microscopy, the effects of GSC on neighboring cell fates could be observed.

[7] The data collected from the whole-exome sequencing, as well as the phenotypical presentation of SAMS, indicates that in mammals, the goosecoid protein is involved with the regulation and migration of neural crest cell fates and other mesodermal patterning, notably joints like the shoulders and hips.

[15] A mutation in the GSC gene causes short stature, auditory canal atresia, mandibular hypoplasia, and skeletal abnormalities (SAMS).

SAMS was previously thought to be an autosomal-recessive disorder but studies with molecular karyotyping and whole-exome sequencing (WES) has shown otherwise.

Mutations to the Gsc gene in humans can lead to a condition known as SAMS syndrome, characterized by short stature, auditory canal atresia, mandibular hypoplasia, and skeletal abnormalities.

[19] Furthermore, high levels of GSC expression in cancer cells correlates with poor survival rates and thus can be used as a prognostic tool.

Therefore, GSC “primes cells for the expression of aggressive phenotypes[19]” and “may be the most potential biomarker of drug response and poor prognosis.