Lyn, also known as Lck/yes-related protein tyrosine kinase, belongs to the Src family kinases (SFKs). It plays numerous biological functions, such as modulating receptor-mediated intracellular signaling and intercellular communication, and is essential in immunoreceptor signaling pathways [2,3]. Lyn is involved in multiple pathways like the IgE/FcεRI signaling pathway regulating allergy [3], and has a role in the development and function of B lymphocytes and myeloid immune cells [2,4,5].

Lyn-deficient mouse models have revealed its significance in various disease conditions. Lyn-/-mice develop an SLE-like disease with plasma cell hyperplasia, highlighting its role in tightly regulating signaling within B cells in systemic lupus erythematosus (SLE) [4,5,7]. In sepsis-associated acute kidney injury (SA-AKI), Lyn protected against renal tubular injury in a cecal ligation and puncture (CLP) induced AKI mouse model by inhibiting STAT3 phosphorylation and cell apoptosis [1]. Also, pharmacological inhibition or genetic depletion of Lyn in cells blocked the secretion of Dengue and Zika infectious particles, indicating its role in flavivirus egress [6].

In conclusion, Lyn is a crucial regulator in multiple biological processes and diseases. Model-based research, especially using Lyn knockout mouse models, has been instrumental in uncovering its role in diseases such as SLE, SA-AKI, and flavivirus-related conditions, providing insights into potential therapeutic targets.