Recently, an increasing number of studies have observed abnormal expression of ITGA2 in various malignancies, exerting a significant influence on multiple facets of tumor initiation and progression, encompassing pancreatic cancer, gastric cancer, liver cancer, breast cancer, and glioma (6–9) as well as it has been demonstrated that loss of ITGA2 leads to reduced proliferation, invasion, and adhesion of glioblastoma cells, which suggested that ITGA2 emerged as a potential therapeutic target in glioblastoma (10). This evidence concerns the gene ITGA2 and neoplasm.