Stk24, also known as MST3, belongs to the germinal center kinase III subfamily. It is involved in multiple biological functions and associated pathways. For example, it may play a role in regulating cell proliferation, immune microenvironment modulation, and is associated with pathways like AKT-PD-L1, STAT3/VEGFA, and NLRP3 inflammasome regulation [2,4,5,3]. Genetic models such as gene knockout (KO) or conditional knockout (CKO) mouse models are valuable for studying its functions.

In KO/CKO mouse models, deletion of Stk24/25 in endothelial cells led to defects in vascular patterning during development and formation of cerebral cavernous malformation (CCM) lesions postnatally [1]. Stk24-deficient mice developed severe high-fat diet-induced metabolic disorders and insulin insensitivity, as Stk24 deficiency in the hematopoietic system promoted NLRP3 inflammasome activation [3]. In the kidney tubules, deficiency of Stk24/25 led to polyuria and increased water consumption due to altered aquaporin 2 (Aqp2) membrane targeting [6].

In conclusion, Stk24 plays essential roles in maintaining normal physiological functions. Model-based research, especially KO/CKO mouse models, has revealed its significance in diseases such as CCM, obesity-associated metabolic disorders, and kidney water balance regulation. Understanding Stk24's functions provides insights into the mechanisms of these diseases and potential therapeutic targets.