This indicates that despite the reported synergy between RAC1b and BRAF V660E in colorectal tumors [27], the altered molecular background that promotes a RAC1b-induced NF-kB-mediated pro-oncogenic response in thyroid cancer remains elusive and probably goes beyond bone-fide genetic alterations in genes such as BRAF, PI3K or RET. This evidence concerns the gene NFKB1 and colorectal neoplasm.