Metap2, also known as methionine aminopeptidase 2, is an intracellular metalloprotease. It plays a critical role in regulating lipid metabolism, energy balance, and protein synthesis. It is involved in angiogenesis and protein synthesis processes, making it important for normal physiological function [1,3,4]. Genetic models, such as KO/CKO mouse models, are valuable for studying its functions.

In a mouse model of ciliopathy (Thm1 conditional knockout mice), Metap2 inhibitor administration reduced daily food intake, body weight, and improved metabolic indices like blood glucose, insulin, and leptin levels. It also decreased gonadal adipose depots and adipocyte size and improved liver morphology, suggesting Metap2's role in ciliary-mediated obesity [5]. In obese mice, Metap2 inhibition decreased body weight and fat mass and increased lean mass, with its anti-obesity activity mediated through direct action on brown adipocytes by enhancing β-adrenergic-signaling-stimulated activities [2].

In conclusion, Metap2 is essential for processes like lipid metabolism, energy balance, and angiogenesis. Studies using mouse models have revealed its significance in obesity-related metabolic disorders, suggesting that targeting Metap2 could be a potential therapeutic strategy for ciliary-mediated forms of obesity and other related metabolic diseases.