Beyond BRAF mutations, various additional genomic abnormalities affecting additional genes, can drive melanoma initiation and progression, such as NRAS, KIT, GNAQ, GNA11, and SF3B1. The different molecular pathways responsible for the development and progression of melanomas are extremely complicated and interact with each other (via crosstalk mechanisms) to create resistance to treatment and the progression of cell signaling. The gene discussed is GNAQ; the disease is melanoma.