Interestingly, RSK inhibition was even capable of re-sensitising resistant melanoma cells to vemurafenib treatment to a certain extent, as pre-treatment of the cells with 5 μM BI-D1870 restored response to the BRAFV600E/K inhibitor reflected in a synergistic effect of BRAF/RSK inhibitor combinations (Supplementary Figure 2C). The gene discussed is RPS6KA1; the disease is melanoma.