To exclude the possibility that random DNA breaks induced by Cas9, rather than specific disruption of mutant KRAS allele, are contributing to the specific inhibition of tumor cell proliferation, a CCK-8 cell proliferation assay was performed after treatments with Cas9 and control sgRNAs targeting AAVS1 (the adeno-associated virus integration site 1) and TTN genes. This evidence concerns the gene KRAS and neoplasm.