Aspn, also known as Asporin, is a gene with diverse functions. In the context of endometriosis, it may be a biomarker and is associated with immune infiltration, as its increased expression is related to immune cell infiltration in endometriosis lesions, and it can potentially serve as an immunotherapeutic target [1]. In colorectal cancer, high expression of Aspn in oxaliplatin-resistant patients is closely correlated with poor prognosis, and down-regulation of Aspn can reverse oxaliplatin resistance and promote cell apoptosis both in vitro and in vivo [2]. In gastric cancer, Aspn, along with MATN3, is significantly up-regulated, and their interaction may drive cancer progression via the epithelial-mesenchymal transition (EMT) pathway [3]. In osteoporosis, Aspn synergizes with HAPLN1 to inhibit the osteogenic differentiation of bone marrow mesenchymal stromal cells and extracellular matrix mineralization of osteoblasts and promote osteoclastogenesis [4].

Although no gene knockout (KO) or conditional knockout (CKO) mouse models are explicitly mentioned in the provided abstracts, these findings across different disease conditions suggest that Aspn plays crucial roles in various biological processes related to disease development.

In conclusion, Aspn is involved in multiple disease-related biological processes, including immune regulation in endometriosis, chemoresistance in colorectal cancer, cancer progression in gastric cancer, and bone metabolism in osteoporosis. Understanding Aspn's functions through in vivo studies, potentially including KO or CKO mouse models in future research, could provide valuable insights into disease mechanisms and therapeutic strategies for these diseases.