Tmsb4x, also known as Thymosin beta 4 X-linked, is an important regulator in immune and inflammation responses, and is involved in actin cytoskeleton remodeling [3,8]. It may play a role in various biological processes, such as cell differentiation, immune response modulation, and tumor-related processes [3,4,5,6,7,9,10].

In non-small cell lung cancer (NSCLC), higher Tmsb4x expression is associated with poorer disease-free survival (DFS) and overall survival (OS) post-surgery, and it may facilitate immune evasion by influencing dendritic cell activation [1]. In hepatocellular carcinoma (HCC), Tmsb4x promotes cell proliferation, migration, invasion, and represses ferroptosis, being involved in inflammation-associated ferroptosis [2]. In septicemia, decreased Tmsb4x expression leads to increased inflammation and reduced dendritic cell proportion, while upregulated Tmsb4x promotes mononuclear cell to dendritic cell differentiation [3]. In colorectal cancer, TMSB4X-high expression in the tumor region is a potential marker [5]. In glioma, TAGLN2 K40succ regulates TMSB4X to promote angiogenesis and tumor growth [6]. In endometriosis, circPIP5K1A accelerates progression via the miR-153-3p/TMSB4X axis [10].

In conclusion, Tmsb4x is involved in multiple biological functions including immune response, cell proliferation, and differentiation. Its dysregulation is associated with various diseases such as NSCLC, HCC, septicemia, colorectal cancer, glioma, and endometriosis. Research on Tmsb4x using in vivo models helps to understand its role in these disease processes, providing potential targets for diagnosis and treatment.