KRAS is an oncogene that encodes the K-Ras protein, a key component of the RAS/MAPK signaling pathway. The K-Ras protein plays an important regulatory role in various cellular processes, including cell growth, proliferation, maturation, and differentiation. KRAS gene mutations are a common cause of cancer, with approximately 30% of cancer patients harboring KRAS mutations. These mutations are predominantly single-nucleotide missense mutations, with over 80% occurring at the 12th amino acid residue (G12), particularly the KRAS G12D mutation, which is very common in lung and pancreatic cancers. The G12D mutation enhances the activity of the K-Ras protein, leading to uncontrolled cell growth and division, thereby promoting tumor formation. The K-Ras protein is highly conserved between mice and humans, with only differences at the 132nd and 187th amino acid residues^[1-2].

The SFTPC gene encodes surfactant protein C (SP-C), one of the four major proteins that make up surfactant. Surfactant is a mixture of lipids and proteins that coats the surface of lung tissue, reducing respiratory resistance. It is produced and secreted by alveolar cells, and its main function is to maintain the stability of lung tissue by reducing the surface tension of lung fluid. In addition, SP-C protein is involved in lung development and function, including alveolar formation, airway remodeling, and immune defense. The SFTPC gene is expressed primarily in the lung, with the highest expression in the lower lobes, right lung, upper lobes, left upper lobes, and visceral pleura. It is also expressed at lower levels in other tissues. Type II alveolar cells are the main producers and secretors of surfactants, and the SFTPC gene is highly expressed in these cells, making it a specific marker of this cell type.

The KS (inducible) mouse is an induced lung cancer model that is constructed by crossing LSL-K-ras G12D mice (Catalog number: C001064), a conditional over-expressing K-Ras G12D mutant gene mouse strain, and Sftpc-MerCreMer mice (Catalog number: C001501), a type II alveolar cell-specific Cre recombinase expressing mouse strain, and then inducing with tamoxifen. Tamoxifen can trigger sequence recombination between loxP sites mediated by Cre recombinase in the type II alveolar cells of the offspring mice, resulting in the specific deletion of the Loxp-Stop-Loxp (LSL) gene silencing element in the type II alveolar cells, thereby enabling the K-Ras G12D mutant gene to be selectively expressed in the lung tissue. Internal data indicates that the model may exhibit slight expression leakage in the absence of tamoxifen induction, leading to the occurrence of a small number of pulmonary adenomas.