In thyroid cancer, the BRAF V600E mutant promotes cell movement through the nuclear factor (NF)-κB pathway as demonstrated in WRO and KTC-3 cell lines in vitro,106 or by mediating hypomethylation and subsequent overexpression of the gene encoding WAS/WASL-interacting protein family member 1 (WIPF1), as demonstrated in K1, OCUT1 and FTC133 cells in vitro and K1 cells in vivo.107 In the Caco-2 colorectal cancer cell line, BRAF V600E represses E-cadherin and enhances the activity of Rho GTPases.102 Other evidence also supports a role for BRAF mutants in EMT-associated tumour invasion.108,109. The gene discussed is BRAF; the disease is neoplasm.