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. This evidence concerns the gene YAP1 and melanoma.