In mouse xenograft assays, a K-RAS G12V/K147L double mutant that cannot be ubiquitylated showed significantly decreased tumor mass and volume, compared to oncogenic K-RAS G12V expressing isogenic control cells, suggesting a critical role of Lys147 monoubiquitylation, or possibly through other modifications (e.g., acetylation, methylation), in tumor progression (Sasaki et al., 2011). This evidence concerns the gene KRAS and neoplasm.