While canine MTC may be similarly driven by RET signaling (although, unlike humans, no driver mutations nor fusions were detected in our dataset), canine FTC do not appear to rely on RAS/RAF signaling and display a heterogenous mutational landscape, employing a variety of processes for oncogenesis (including ERBB2 and PI3K, as well as dysregulation of epigenomic and DNA repair pathways). This evidence concerns the gene ERBB2 and medullary thyroid gland carcinoma.