Tnfaip8, also known as Tumour necrosis factor (TNF)-α-inducible protein 8, is the founding member of the TIPE family. It acts as an anti-apoptotic protein, influencing multiple biological processes such as cell proliferation, metastasis, invasion, angiogenesis, drug resistance, and immune response through multiple signalling pathways like PI3K-AKT, mTOR-Akt-ULK1, and autophagy signals. It is of great importance in maintaining immune homeostasis and is associated with the development of various tumours and inflammatory diseases. Genetic models can help in further understanding its role [1,3,4,6,7,8,9].

In a streptozotocin-induced mouse model of diabetic retinopathy, overexpression of Tnfaip8 using an adeno-associated virus vector led to decreased a/b-wave amplitude, reduced retinal thickness, aggravated pathological abnormalities, increased avascular area, leukostasis, and up-regulated inflammatory factors in the retina, indicating its role in the pathogenesis of diabetic retinopathy [2]. In the context of kidney fibrosis, in vivo gain-or loss-of Tnfaip8 in a model of obstructive nephropathy either prevented or aggravated renal fibroblast apoptosis. Exosomal-Tnfaip8 promoted p53 ubiquitination and degradation, inhibiting fibroblast apoptosis and inducing proliferation [5].

In conclusion, Tnfaip8 plays crucial roles in maintaining immune homeostasis, tumour development, and inflammatory diseases. Studies using mouse models have revealed its functions in diabetic retinopathy and kidney fibrosis. Understanding Tnfaip8's functions can potentially offer novel therapeutic strategies for these and other related diseases.