A group of studies, mostly in melanoma but also in breast and thyroid cancer, linked NRG1-induced ErbB3 activation to a paracrine effect and to a remodelling of the tumour microenvironment following exposure to BRAF and MEK inhibitors involving stromal fibroblasts as the main source of NRG-1 mediated PI3k/AKT activation [4,20,37,38]. The gene discussed is BRAF; the disease is thyroid gland carcinoma.