Their results showed that each mutation generates a distinct signaling network signature which affects the expression and phosphorylation of genes with a role in promoting oncogenic CRC signaling and tumorigenesis, the pre-eminent example being double cortin-like kinase-1 (DCLK1), which was overexpressed in all variants of codon 12 KRAS mutant cells but not in G13D cells [87]. Here, KRAS is linked to colorectal carcinoma.