One-third of all human cancers are attributable to mutations in RAS. Induction of oncogenic RAS during tumorigenesis leads to metabolic reprogramming and enhanced proliferation or senescence. These profound phenotypic changes require adaptations in gene expression, RNA processing, and protein synthesis. To investigate core drivers of this transformation, we analysed nuclear protein expression in IMR90 RAS cells and IMR90 Control cells 6 days after induction of HRASG12V.