For the type-A probe (targeting all known isoforms, and hence representing expression of KRAS in general), there was down-regulation of KRAS in CRC tissue compared to normal tissue (p = 0.0002) irrespective of the KRAS mutation status or tumor staging and the magnitude of differential expression was not different based on the KRAS mutation status (interaction p = 0.82) or tumor stage (interaction p = 0.33). Here, KRAS is linked to colorectal carcinoma.