BRAF and melanoma: For instance, scRNA-seq studies of melanoma cultures exposed to different treatments showed induction of distinct transcriptional programs that could lead to drug resistance; BRAF-mutant melanoma cells resistant to BRAF inhibitor alone showed a high cell cycling and proliferative phenotype while those resistant to combination BRAF/MEK inhibitors showed signatures of high translational activity, PI3K pathway activation and alternate MAPK pathway reactivation.52