In healthy cells, KRAS is an on/off switch that regulates cell growth by binding GTP, which is then converted to GDP. KRAS can, however, become fixed in the "on" position when the gene is mutated, resulting in uncontrolled cell growth. Although mutant KRAS has been extensively studied and is prevalent in cancer, it remains a challenging therapeutic target due to the lack of traditional druggable pockets on its surface. Recent discoveries of potent covalent inhibitors of the KRASG12C mutant have sparked new interest in small molecules targeting KRAS. It is in this context that Proteolysis TArgeting Chimeras (PROTACs) a new and promising method for drug discovery presents itself as one possible solution.