CLK2 promoted the inclusion skipping at exon 11a of mesenchymal-type ENAH in luminal breast cancer cells through the modulation of RBFOX2 as opposed to SRSF1.42 The usage of ENAH exon 11a affected by CLK2 subsequently implied cell growth, migration, and invasion in breast cancer.42 This evidence concerns the gene ENAH and breast carcinoma.