The Fas cell surface death receptor (FAS), also known as CD95 or TNFRSF6, is a type I transmembrane protein in the tumor necrosis factor receptor superfamily ^[1]. It plays a key role in apoptosis by transmitting signals that initiate programmed cell death. Expressed across various tissues such as immune cells, liver, heart, and skin, FAS regulates cellular homeostasis. Upon binding with its ligand (FASL), FAS oligomerizes to form the death-inducing signaling complex (DISC), activating caspases that execute apoptosis. This is crucial for immune homeostasis, tissue maintenance, and removing damaged or infected cells. Dysregulated FAS-mediated apoptosis can lead to autoimmune disorders (e.g., autoimmune lymphoproliferative syndrome) or contribute to cancer development by enabling uncontrolled cell proliferation ^[1-3]. The MRL/MpJ Strain (Murphy Roths Large), derived from a complex cross between several strains (LG/J, AKR/J, C3H/Di, C57BL/6), was established for autoimmune disease research. They serve as controls in studies of the MRL/MpJ-Faslpr strain, a mouse model with premature termination of gene transcription and abnormal mRNA splicing due to lymphoproliferation (lpr) spontaneous mutation of the Fas gene, which develops lupus-like autoimmune disease ^[4]. MRL/MpJ mice are vital in studying autoimmune conditions (e.g., Sjögren syndrome, autoimmune arthritis, lupus erythematosus, hearing defects) and are notable for their scarless tissue regeneration capabilities. This makes them valuable models for research in tissue regeneration, wound healing, autoimmune diseases, muscle dystrophy, and hearing loss ^[4-6]. The MRL/MpJ-Fas knockout (KO) mouse model, generated via targeted deletion of the Fas gene in MRL/MpJ mice, provides a critical tool for investigating the role of FAS in autoimmune pathologies. This model furnishes a critical system for elucidating the etiology of systemic lupus erythematosus (SLE) and identifying potential therapeutic targets within the FAS signaling cascade for the treatment of autoimmune disorders.

3110082I17Rik is located on chromosome 5 of mice. Nuclease Technology was used to design sgRNA; 3110082I17Rik knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Gsto2 is located on chromosome 19 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Gsto2 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Fas is located on chromosome 19 of mice. Nuclease Technology was used to design sgRNA; Fas knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Fas is located on chromosome 19 of mice. Nuclease Technology will be used to design sgRNA; Fas knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Fas is located on chromosome 19 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Fas conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.