Role of KRAS gene in the diagnosis and treatment of colorectal cancer Zrinka Madunić Colorectal cancer (CRC) is a heterogeneous disease at the cellular and molecular level. Kirsten rat sarcoma virus (KRAS) gene is a frequently mutated oncogene in CRC, with mutations present in approximately 40% of all CRC cases. Mutations result in constitutive activation of the KRAS protein, which acts as a molecular switch to continuously stimulate downstream signalling pathways, promoting cell proliferation and survival, leading to tumorigenesis. Patients whose CRC contains cells with mutated KRAS have a worse prognosis overall. There are various laboratory methods for mutation detection, emphasizing real-time PCR analysis, Therascreen KRAS kit, and other methods such as StripAssay and SNaPshot. Due to the presence of KRAS mutations, this group of CRC patients requires more precise therapies. The KRAS protein was historically considered inaccessible to targeted therapy until the development of KRASG12C-specific inhibitors. The immunosuppressive environment of KRAS mutated CRC explains the limitations of immunotherapy, but also highlights potential therapeutic approaches such as adoptive transfer of T lymphocytes targeting the KRAS mutant or vaccines to neutralize the KRAS protein. These promising inhibitors may provide new strategies for the treatment of KRAS-mutated CRC.