In the TGF‐β pathway, mutations in TGFBR2, ACVR1B, and SMAD2‐4 promote tumor progression and enhance invasiveness through epithelial‐to‐mesenchymal (EMT) transition and are linked to resistance against therapies such as BRAF/MEK inhibitors, EGFR tyrosine kinase inhibitors (TKIs), and SMAD4‐targeted treatments [33, 34]. The gene discussed is BRAF; the disease is neoplasm.