In the present work, we clearly demonstrated in a large series of PTC – and further confirmed by data emerging from a large-scale meta-analysis of microarray studies in thyroid tumors – an increased expression/activity of AHR, independently from its nuclear dimerization partner ARNT and its repressor AHRR, but strictly related to a constitutive active MAPK/ERK pathway. The gene discussed is AHR; the disease is thyroid tumor.