Fabp5, also known as epidermal FABP, is an intracellular chaperone of fatty acid molecules. It regulates lipid metabolism and cell growth, and is involved in pathways such as mTORC1 signaling, PPARγ signaling, and NF-κB signaling. Fabp5 plays a crucial role in various biological processes, including immune regulation, inflammation, and cell proliferation, and is associated with multiple diseases such as cancer, allergic asthma, and psoriasis [1,2,3,4]. Genetic models, like KO and CKO mouse models, have been instrumental in studying Fabp5's functions.

In KO mouse models, macrophage-specific Fabp5 deficiency decreases immunosuppressive molecule expression in tumour-associated macrophages, enhancing T-cell-dependent antitumour immunity and diminishing HCC growth [1]. In myeloid-specific Fabp5-deleted mice, OVA-induced allergic airway inflammation is exacerbated due to increased alternatively activated macrophages [2]. Global and keratinocyte conditional knockout of Fabp5 in mice attenuates psoriatic symptoms by reducing skin recruitment of Ly6G+ neutrophils [3]. In contrast, in some cancers, Fabp5 promotes tumour progression. For example, in cervical cancer, it promotes lymph node metastasis by reprogramming fatty acid metabolism [5]. However, in colorectal cancer, it suppresses tumour progression via mTOR-mediated autophagy by decreasing FASN expression [6].

In conclusion, Fabp5 has diverse functions in regulating lipid metabolism, immune responses, and inflammation. Fabp5 KO/CKO mouse models have significantly contributed to understanding its role in diseases like cancer, allergic asthma, and psoriasis, providing potential therapeutic targets for these conditions.