Itga4, also known as Integrin Subunit Alpha 4, is a member of the integrin protein family. Integrins are cell adhesion molecules that play crucial roles in cell-cell and cell-extracellular matrix interactions. Itga4 is involved in multiple biological processes such as cell adhesion, migration, and immune regulation, and is associated with pathways like PI3K-Akt and TSC-mTOR [5].

In pancreatic cancer, the LAMA5/ITGA4 axis in cancer-associated fibroblasts (CAFs) is responsible for CAF-mediated acinar-to-ductal cell transdifferentiation, highlighting its role in pancreatic carcinogenesis [1].

In chronic lymphocytic leukemia (CLL), hypermethylation at ITGA4 gene CpG sites (1, 2, 3) is a characteristic feature [2].

In aging muscle, the chemokine/ITGA4 interaction directs iPSC-derived myogenic progenitor migration to injury sites for regeneration [3].

In inflammatory bowel disease, associated variants of ITGA4 are correlated with expression changes in response to immune stimulus [4].

In gastric cancer, ITGA4 promotes tumor proliferation and migration, and is related to poor prognosis [5,7].

In colorectal cancer, low ITGA4 expression is related to poor prognosis, and ITGA4 might participate in the inflammatory reaction and inflammatory tumor transformation process [6].

In glioma, GAS41 promotes ITGA4-mediated PI3K/Akt/mTOR signaling pathway and glioma tumorigenesis [8].

In conclusion, Itga4 is essential for multiple biological processes including cell adhesion, migration, and immune regulation. Studies, especially those using gene-based models in various diseases like pancreatic cancer, leukemia, muscle regeneration-related conditions, inflammatory bowel disease, gastric cancer, colorectal cancer, and glioma, have revealed its significant roles in disease development and progression. These findings provide potential insights for disease treatment and prevention targeting Itga4.