Since solTNF has been implicated as one of the key exogenous factors that promotes resistance to MAPKi by BRAF-mutant melanoma [9, 10], addition of NF-κB signaling pathway inhibitors (e.g. BMS-345541) or TNF antagonists (e.g. etanercept, adalimumab, infliximab) has been proposed to enhance MAPKi-based therapies to improve their clinical efficacy. The gene discussed is BRAF; the disease is melanoma.