BRAF and thyroid nodule: In the context of thyroid nodules with AUS, the BRAF V600E mutation is particularly significant. The mutation leads to persistent activation of the MAPK/ERK pathway, which promotes cell proliferation, differentiation, and survival. Specifically, BRAF V600E protein activates mitogen-activated protein kinase kinase (MEK), which in turn phosphorylates and activates ERK. Activated ERK translocates to the nucleus, where it phosphorylates c-Myc and c-Jun thereby regulating the expression of genes involved in cell cycle progression [10-12].