To evaluate the importance of RSK signalling in the resistant melanoma cells, we used the specific, ATP-competitive pan-RSK inhibitor BI-D1870, which did not affect the activating phosphorylation of RSK at Threonine359/Serine363, but efficiently reduced phosphorylation of the RSK target YB-1 in the vemurafenib resistant melanoma cells, both in the presence and absence of the BRAFV600E/K inhibitor (Figure 2A). The gene discussed is RPS6KA1; the disease is melanoma.