Transforming growth factor-β (TGF-β), as the main inducer of EMT, induces alternative splicing of TGF-β-activated kinase 1 to reject exon 12 during EMT.87 In EMT, the alternative splicing of cluster of differentiation 44 (CD44) has been changed through the regulation of the splicing factor ESRP1, which determines the interaction between CD44 and cell surface receptor tyrosine kinases.88 The generated CD44s could promote the occurrence and development of the EMT of breast cancer cells. The gene discussed is CD44; the disease is breast carcinoma.