Although it is beyond the scope of this manuscript, several mechanistic hypotheses may explain the connections between KRAS mutation, cyclin A2 elevation and PLK1 inhibitor sensitivity: Potentially, upon glutamine (Gln) deprivation, KRAS-driven cancer cells bypass a late G1 Gln-dependent cell cycle checkpoint and enter S-phase, followed by cell cycle arrest due to insufficient nucleotide biosynthesis [35]. This evidence concerns the gene PLK1 and cancer.