K-RAS is currently the most promising biomarker in colorectal carcinoma (CRC). Functionally, the RAS protein plays a key role in the EGFR signaling pathway. In around 30-40% of all patients with CRC a mutated K-RAS gene can be found in the tumor, while 60-70% of patients express a wild-type K-RAS gene in the tumor. The K-RAS status is now generally regarded as a predictive factor for the response to anti-EGFR therapy: patients with the mutated K-RAS gene derive no benefit from treatment with the anti-EGFR antibodies cetuximab or panitumumab. The VEGF antibody bevacizumab, by contrast, seems to be efficacious with both wild-type K-RAS and mutated K-RAS - though larger-scale trials must still be carried out here.