Because BRAF and the other RAF kinases were putative downstream signal transducing molecules for RET/PTC, and because mutations in BRAF and RAS, and rearrangements in NTRK and RET/PTC are largely mutually exclusive in human PTC samples, it was suggested that the RAS/RAF/MEK pathways might represent a linear cascade whose activation promotes thyroid cancer formation (Kimura et al, 2003; Soares et al, 2003). Here, RAF1 is linked to thyroid gland carcinoma.