Lix1l, or Limb expression 1-like protein, is involved in post-transcriptional gene regulation. It has been associated with multiple biological processes and disease-related pathways. Genetic models, such as knockout mice, have been crucial in studying its functions [1,2,3].

Lix1l knockout mice studies revealed that Lix1l deficiency alleviates cholestatic liver injury by inhibiting bile acid synthesis, as LIX1L functions as a link between BA/Egr-1 and miR-191-3p/LRH-1 signaling [1]. Also, Lix1l deletion in mice inhibits hepatic lipid accumulation, inflammation, and fibrosis as well as adipocyte differentiation by downregulating CD36, alleviating metabolic dysfunction-associated steatohepatitis (MASH) and associated hepatocellular carcinoma (HCC) progression [2]. In addition, Lix1l deficiency in vivo significantly attenuated liver cancer initiation in mice, and LIX1L knockdown up-regulated fructose-1,6-bisphosphatase (FBP1) expression to reduce glucose consumption and lactate production [3].

In conclusion, Lix1l plays important roles in liver-related diseases including cholestatic liver injury, MASH, and HCC. Gene knockout mouse models have been instrumental in uncovering these functions, highlighting Lix1l as a potential therapeutic target for these diseases.