In the light of its characteristics that KRAS function as a “binary functional molecular switch” cycling between the inactive GDP-bound state and the active GTP-bound state [40–42], we determined active GTP-binding KRAS in CRC cells using a K-Ras Activation Assay Kit, and found that the overexpression of RNF141 raised the level of active GTP-bound KRAS and the knockdown of RNF141 in turn decreased the active GTP-bound KRAS. Here, KRAS is linked to colorectal carcinoma.