JAML, short for Junctional Adhesion Molecule-Like Protein, is a protein-coding gene. It plays diverse roles in multiple biological processes, associated with various signaling pathways such as SIRT1-mediated SREBP1, PI3K-AKT-mTOR, and is involved in T-cell activation, lipid metabolism, and immune-related processes [1,3,4,5]. Genetic models, especially gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable for studying JAML's functions.

In DKD, podocyte-specific deletion of Jaml ameliorated podocyte injury and proteinuria, revealing its role in promoting DKD by modulating podocyte lipid metabolism [1]. In AKI, macrophage-specific and tubular cell-specific Jaml conditional knockout mice demonstrated that JAML promoted AKI mainly via a macrophage-dependent mechanism [2]. In cancer, endothelial-specific knockout of JAML in mice effectively inhibited tumour growth through normalizing tumour blood vessels, suggesting JAML promotes tumour progression by angiogenesis [6].

In conclusion, JAML is involved in multiple biological functions including lipid metabolism, immune-mediated processes, and cancer-related angiogenesis. The use of Jaml KO/CKO mouse models has provided crucial insights into its role in DKD, AKI, and cancer, highlighting its potential as a therapeutic target for these diseases.