FOCAD, also known as KIAA1797, encodes a novel focal adhesion protein. It functions as a tumor suppressor in various cancers and is involved in pathways like the SKI mRNA surveillance pathway. FOCAD is crucial for maintaining liver homeostasis and impacts processes such as microtubule assembly and cell cycle progression [2,3,4]. Genetic models, including zebrafish lacking focad and gene knockout in human hepatic cell lines, have been used to study its functions [1].

In the context of diseases, loss of FOCAD in zebrafish phenocopied pediatric liver cirrhosis in humans, revealing its importance in the SKI mRNA surveillance pathway. Deficiency in FOCAD compromises this pathway by reducing levels of RNA helicase SKIC2 and its cofactor SKIC3. FOCAD knockout hepatocytes showed lowered albumin expression, signs of persistent injury, and CCL2 overproduction [1]. In astrocytic gliomas, FOCAD loss was associated with inferior patient outcomes, as it enhanced microtubule assembly and accelerated G2/M phase progression [3]. In gastric cancer, FOCAD was found to be a tumor suppressor, with its down-regulation promoting cell proliferation and migration [2].

In conclusion, FOCAD has essential functions in maintaining liver homeostasis and acts as a tumor suppressor in multiple cancers. Gene knockout and other genetic models have been instrumental in revealing its role in specific biological processes and disease conditions, such as pediatric liver cirrhosis and gliomas, providing potential therapeutic intervention points.