Importantly, reduced activity of ERBB3, AXL, EPHA2, and EGFR was also observed after knockout of SLC35B2 in non-engineered Vemurafenib-resistant SKMEL28R melanoma cells with MITFlow/AXLhigh phenotype and high intrinsic YAP1/TAZ activity (Fig. 6e and Supplementary Fig. 7), indicating that the effect of SLC35B2 on RTK signaling was not specific for engineered YAP1 activation. The gene discussed is EGFR; the disease is melanoma.