The objective of the present study is to help unravel the genetic dynamics of feline thyroid tumors, with a particular focus on the most commonly activated signaling pathways observed in human TC (MAPK and mTOR pathways), by assessing the immunohistochemical expression of their phosphorylated downstream effectors (ERK, S6, and AKT), and by investigating potential mutations in key driver genes (BRAF, HRAS, NRAS, and KRAS). Here, KRAS is linked to thyroid tumor.