Fbp1, also known as fructose 1,6-bisphosphatase 1, is a key enzyme in gluconeogenesis. It plays a crucial role in maintaining metabolic homeostasis, with its activity influencing carbohydrate metabolism pathways. Genetic models, such as knockout (KO) and conditional knockout (CKO) mouse models, have been instrumental in studying its functions.

In liver-related research, hepatocyte-specific Fbp1 deletion in mice leads to steatosis, activation and senescence of hepatic stellate cells (HSCs), and promotes tumour progression, indicating Fbp1 as a metabolic tumour suppressor in liver cancer [1]. In Kras-driven lung cancer, loss of Fbp1 in natural killer (NK) cells causes their dysfunction by inhibiting glycolysis, showing its role in NK cell-tumour cell interactions during tumour development [2]. In keratinocytes, Fbp1 promotes differentiation and inhibits proliferation, and its deficiency in mice facilitates psoriasis-like skin lesions development [3]. In non-small cell lung cancer (NSCLC), overexpression of Fbp1 decreases the proportion of CD133-positive cells and weakens tumorigenicity by promoting the ubiquitination and degradation of Notch1 intracellular domain [4].

In conclusion, Fbp1 is essential for metabolic regulation and plays significant roles in multiple disease conditions. KO/CKO mouse models have been vital in uncovering its functions in liver cancer, lung cancer, psoriasis, and NSCLC, highlighting its potential as a therapeutic target in these diseases.