We previously reported that murine (TPO-Cre/HRASG12V/TP53flox/flox) poorly differentiated thyroid cancers developed acquired resistance to FTIs associated with mutations in Nf1 and Gnas, which recapitulated FTI resistance when introduced into HRAS-mutant thyroid cancer cells.(10) We hypothesized that distinct co-mutations occurring across cancer lineages might be responsible for the inconsistent responses to FTIs. Here, HRAS is linked to thyroid gland carcinoma.