Cmip, also known as C-Maf-inducing protein, is involved in multiple biological processes and disease-related pathways. 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-related diseases [2]. It is also associated with Herceptin resistance in HER2-positive gastric cancer cells [3], and the development of non-alcoholic fatty liver disease (NAFLD) through the regulation of the Gbp2-Pparγ-CD36 axis [4].

In the context of disease, CMIP SNPs and their haplotypes are linked to dyslipidemia and clinicopathologic features of IgA nephropathy [5]. In glioma and gastric cancer, CMIP promotes cell proliferation, metastasis, and is considered oncogenic [6,7]. In the study of free fatty acid biology, CMIP protects cells from FFA exposure by modulating Akt signaling [8]. Moreover, CMIP haploinsufficiency may be the cause of syndromic autism spectrum disorder in some patients [9], and WT1 represses CMIP transcription in podocytes [10].

In conclusion, Cmip is a multifunctional protein involved in various biological processes and disease conditions. Studies, especially those using genetic models such as gene knockout or conditional knockout mouse models, have revealed its roles in T-cell regulation, podocyte function, cancer development, lipid-related diseases, and neurological disorders. Understanding Cmip's functions provides potential therapeutic targets for these diseases.