Pik3cd, encoding the catalytic p110δ subunit of phosphoinositide 3-kinase (PI3K), is crucial in the PI3K-AKT-mechanistic target of rapamycin pathway. This pathway is involved in various biological processes such as cell growth, differentiation, and immune response [2,7].

In breast carcinoma, Pik3cd expression is associated with prognosis, epithelial-mesenchymal transition (EMT), and tumor immune infiltration. In gastric carcinoma, its overexpression promotes tumor development, and genetic silencing retards proliferation and migration both in vitro and in vivo [1,4]. In glioblastoma, knockout of Pik3cd in cell lines reduces migration, invasion, and colony-forming ability, and negates tumorigenesis in nude mice, potentially acting through cytoskeletal proteins PAK3 and PLEK2 [5]. In colorectal cancer, overexpression of Pik3cd promotes cell growth, migration, and invasion by activating AKT/GSK-3β/β-catenin signaling [6]. In abnormal retinal angiogenesis, editing genomic Pik3cd in a mouse model significantly reduces pathological angiogenesis [3]. In addition, in diabetic retinopathy, Pik3cd is involved in promoting microvascular endothelial cell proliferation, migration, and angiogenesis [8].

In conclusion, Pik3cd plays essential roles in multiple biological processes and disease conditions. Studies using gene knockout models, such as in glioblastoma and abnormal retinal angiogenesis mouse models, have revealed its role in tumorigenesis and angiogenesis. These findings suggest that Pik3cd could be a potential therapeutic target for various diseases including carcinomas, glioblastoma, and diseases related to abnormal angiogenesis [3,5].