The role of extracellular signal-regulated kinase 1/2 (ERK1/2) in signaling pathways in cells is crucial for cell proliferation. Within specific types of cancers, a member of this pathway, BRAF, is mutated at the valine (V)600 position so that this pathway is continuously activated, leading to uncontrolled proliferation. A docking site in ERK1/2 is of interest for inhibitors to control activation of downstream proteins responsible for transcription.1 A compound has been developed to target a substrate docking site and was found to target a specific cysteine2. This residue has been mutated via CRISPR CAS9 in both ERK1 and ERK2 and the proposed studies investigate the effects the ERK1/2 cysteine mutations have on A375 cell melanoma cells regarding cell signaling and proliferation.