CA199, a sialylated Lewis antigen, further contributes to TD formation through multifaceted mechanisms (29, 30): (1) promoting epithelial-mesenchymal transition via downregulation of E-cadherin and upregulation of vimentin; (2) fostering immune evasion by binding to selectins on immune cells, thereby suppressing cytotoxic T-cell activity (31); and (3) enhancing angiogenesis through VEGF-mediated pathways (32). The gene discussed is VIM; the disease is thanatophoric dysplasia.