Blk, also known as B-cell lymphocyte kinase, is a member of the SRC family nonreceptor tyrosine kinase. It is involved in the B-cell receptor (BCR) signaling pathway, playing a crucial role in B cell development and function [6]. BLK is also associated with TLR/IL-1R signaling and the innate antiviral response, which are essential for immune responses against pathogens [1,7].

BLK-deficient mice produce less inflammatory cytokines and are more resistant to death upon IL-1β challenge, highlighting its positive regulatory role in TLR/IL-1R-mediated inflammatory response [1]. Also, BLK-deficient mice exhibit lower serum cytokine levels and higher lethality after VSV infection, suggesting its importance in the innate antiviral response [7]. In addition, polymorphisms in the BLK gene are associated with susceptibility to diseases like systemic lupus erythematosus (SLE), neuromyelitis optica spectrum disorder (NMOSD), and primary Sjögren's syndrome (pSS) [2,3,4]. In diffuse large B-cell lymphoma (DLBCL), BLK expression is associated with a poor prognosis in patients treated with R-CHOP chemotherapy [5].

In conclusion, Blk is vital for B cell-related functions, immune responses, and inflammation regulation. The use of BLK-deficient mouse models has significantly contributed to understanding its role in various disease conditions such as SLE, NMOSD, pSS, and DLBCL, highlighting its potential as a therapeutic target.