The CFH gene encodes complement factor H, a crucial secreted plasma glycoprotein with twenty short consensus repeat (SCR) domains. Its primary function is to regulate the complement system, a vital part of the innate immune response. CFH acts to prevent uncontrolled activation of the complement pathway on healthy host cells and tissues, thereby restricting its destructive action to foreign invaders ^[1]. Gene expression of CFH is notably high in the liver, where it is synthesized and secreted into the bloodstream. It is also expressed in various other tissues, including ocular tissues like the retina and retinal pigment epithelium (RPE), sclera, and ciliary body, as well as in the kidney, lung, and certain immune cells ^[2-4]. The protein binds to C3b, accelerating the decay of alternative pathway C3-convertase and acting as a cofactor for Factor I-mediated inactivation of C3b ^[1-2]. Dysregulation or mutations in the CFH gene are associated with several diseases, including age-related macular degeneration (AMD), a common cause of vision loss characterized by drusen accumulation, atypical hemolytic-uremic syndrome (aHUS), which causes abnormal blood clots and kidney failure, C3 glomerulopathy (C3G), a rare kidney disease, and Membranoproliferative glomerulonephritis (MPGN), particularly type II (also known as Dense Deposit Disease), a group of kidney diseases characterized by inflammation and damage to the kidney's filtering units (glomeruli), often due to complement dysregulation ^[2-4]. The Cfh-KO mouse is a gene knockout model created using gene-editing techniques to knock out the Exon 2~3 of the Cfh gene (the homolog of the human CFH gene) in mice. This model can be used for research into the pathogenic mechanisms of diseases such as age-related macular degeneration, atypical hemolytic uremic syndrome, C3 glomerulopathy, and Type II membranoproliferative glomerulonephritis, as well as for the development of related treatment methods.

Cfh is located on chromosome 1 of mice. Nuclease Technology was used to design sgRNA; Cfh knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Inka1 is located on chromosome 9 of mice. Nuclease Technology will be used to design sgRNA; Inka1 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Cfh is located on chromosome 1 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Cfh conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Gm11992 is located on chromosome 11 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Gm11992 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.