CFB, short for Complement Factor B, is a key component in the alternative complement pathway. It plays a crucial role in the immune response, helping to label target particles for effective clearance. This pathway is essential for the body's defense against pathogens and in maintaining immune homeostasis [4]. Genetic models, such as knockout (KO) mouse models, have been instrumental in understanding CFB's functions.

In diabetic kidney disease, Cfb-knockout mice demonstrated milder tubulointerstitial injury and reduced ceramide biosynthesis. This indicates that CFB deficiency inhibits activation of the complement alternative pathway, attenuating kidney damage by blocking the NF-κB signaling pathway and subsequent ceramide synthesis [1].

In perianal Crohn's disease, a non-synonymous SNP (G252S) in CFB, associated with the disease, led to impaired CFB cleavage, reduced activation of the alternative complement pathway, and decreased pathogen phagocytosis [2].

In lung adenocarcinoma, knockdown of CFB in vitro increased cell proliferation and migration, while overexpression inhibited tumor growth in vivo, suggesting CFB acts as a tumor suppressor through downregulating the Ras/MAPK signaling pathway [3].

In conclusion, CFB is vital in the alternative complement pathway, influencing immune-related functions. Studies using KO mouse models have revealed its significance in diseases like diabetic kidney disease, perianal Crohn's disease, and lung adenocarcinoma, highlighting its potential as a therapeutic target in these disease areas.