In response to BRAF inhibition, melanoma cells and fibroblasts undergo microenvironmental changes that enhance PI3K/AKT survival signaling, allowing tumor cells to evade treatment.465 When treated with Emurafenib, melanoma cells release TGF-β, triggering fibroblasts to increase expression levels of α-smooth muscle actin (α-SMA), neuregulin (NRG), and fibronectin. The gene discussed is ACTA1; the disease is melanoma.