Oncogenic functions of ERBB3 and ERBB4, which can form heterodimers and signal through the PI3K/AKT signaling pathway have not been elucidated yet in detail in relation to the BRAF mutational status in thyroid cancer [41-43]; however, decreased expression of ERBB4 in PTC vs. normal thyroid tissue has been demonstrated in a RT-PCR study whereas ERBB2 and ERBB3 expression was shown to be increased [44]. This evidence concerns the gene ERBB2 and thyroid gland carcinoma.