 This proposed study will utilize the RP2D determined in the Phase III study: trametinib 2mg QD and dabrafenib 150 mg BID. Despite a very promising overall response rate of 81, these patients will also likely go on to develop resistance as a result of new resistance mutations, and given the cooperative signaling network of kinases that sense inhibition of key nodal kinases and induce compensatory responses that offset pharmacological intervention. The study objectives are as follows: Objectives Primary Objective To identify kinases that are differentially expressed pre- and post-treatment with BRAF dabrafenib and MEK trametinib inhibitors, and to determine a kinome signature predictive of resistance to BRAFMEK inhibition in stage IIIIV melanoma Secondary Objectives To explore whether resistance to BRAF and MEK inhibition is associated with new functional mutations in the approximately 150 oncogenes tumor suppressor genes that are assessed in more than 10 of the tumors using NextGen DNA sequencing technology in the subset of patients who co-enroll in LCCC1108, with particular focus on one of five established resistance genes BRAF, NRAS, MEK1, MAP3K8 or COT, and PTEN To determine the overall response rate ORR: complete response partial response as measured via RECISTv1.1 To estimate the duration of ORR as measured via RECISTv1.1 To estimate progression-free survival PFS as defined by RECISTv1.1 To estimate the rate of overall survival OS at 1 year from day 1 of treatment 