Since most ATCs arise as a consequence of accumulating genetic aberrations in a pre-existing well-differentiated thyroid carcinoma, many ATCs harbor mutations usually associated with the development of PTCs and FTCs, such as those targeting the genes BRAF, NRAS, HRAS, KRAS, PIK3CA, E1F1AX, and PTEN [2,11,12,13]. The gene discussed is HRAS; the disease is Ehlers-Danlos syndrome, musculocontractural type.