Interestingly, mutations leading to amino acid substitutions at the position 12 of KRAS (KRASG12X) were more prevalent in CRCs carrying PLK1 PB1 mutations (p < 0.001, Figure 1G), suggesting a potential cooccurrence of KRAS dysfunction and PLK1 PB1 domain abnormalities in CRC. Here, KRAS is linked to colorectal carcinoma.