Similarly to melanoma16, BRAF mutation occurs at early stages of PTC development11, 17. Besides all BRAF oncogenic activities, its single exacerbated stimulation of the MAPK pathway is not sufficient to sustain malignant transformation, resulting in induced senescence18 that confers a barrier to tumor progression19. To bypass BRAF-induced senescence, cells may suffer a second event that allows malignant transformation, as possibly the epigenetic silencing of tumor suppressors DAPK, TIMP320, SLC5A820, 21 and hMLH122 and other BRAF-induced mechanisms that remain to be discovered11. In thyroid cancers, Thyroid-stimulating Hormone (TSH) is more involved in overcoming senescence; while BRAF overexpression suppresses thyroid hormone biosynthesis and leads to elevated TSH levels in vivo 14; it was shown that TSH signaling inhibits BRAFV600E-induced senescence through DUSP623.