KRAS and melanoma: In agreement, analyzing transcriptomic data from previous studies2,15 revealed that the UPR gene signature was significantly enriched in KRAS-mutant cancer cells that underwent an EMT and acquired KRAS independence (Fig. 4e) and in residual BRAF-mutant melanoma resistant to and relapsed after the concurrent treatment with BRAF and MEK inhibitors (Fig. 4f).