However, our results are reasonable based on previous reports related to the interactions of KRAS-SUMO/SUMO-MYC/MYC-KRAS for the following reasons: 1) cell growth in KRAS-mutant CRC is driven by Ubc9, which is a downstream cascade in the SUMOylation pathway [7]; 2) MYC inhibition by dominant-negative MYC mutation eradicates KRAS-mutant GEMM [34]; and 3) hyperactivation of MYC is associated with sensitivity to pharmacological SUMO inhibition in PDAC [35]. The gene discussed is KRAS; the disease is colorectal carcinoma.