Cmip, also known as C-Maf-inducing protein, is involved in multiple biological processes and associated with various diseases. In T cells, it acts as a negative regulator of signaling, influencing proximal signaling and cytoskeletal rearrangement [1]. In podocytes, it can interact with WT1 and target it for proteasome degradation, potentially playing a role in podocyte diseases [2].

In mouse models, intravenous injection of Cmip-siRNA ameliorated non-alcoholic fatty liver disease (NAFLD) pathogenic features in ob/ob mice, indicating that Dnmt1/Tet2-mediated changes in Cmip methylation regulate the Gbp2-Pparγ-CD36 axis, suggesting Cmip as a potential therapeutic target for NAFLD [4]. In human studies, CMIP SNPs and their haplotypes are associated with dyslipidaemia and clinicopathologic features of IgA nephropathy [5]. Also, in cancer, CMIP promotes Herceptin resistance in HER2-positive gastric cancer cells [3], proliferation and metastasis in human glioma [6], and has an oncogenic role in human gastric cancer cells [7].

In conclusion, Cmip is involved in diverse biological functions such as T-cell regulation, podocyte function, and lipid-related processes. Mouse models, especially those using siRNA-mediated knockdown similar to gene-knockout effects, have revealed its potential as a therapeutic target in diseases like NAFLD, and its associations with various cancers and kidney-related diseases. These studies provide insights into the underlying mechanisms of these diseases and potential directions for treatment.