We observed high correlationbetween the extent of Msi overexpression and the change in splicing in luminaltumors, particularly for MSI2. As in mouse NSCs, increasedexpression of Msis was associated with increased inclusion of theERBIN exon and repression of MYO18A exonsplicing, suggesting that Msi-dependent regulation of splicing may be conserved notonly in breast cancer cell lines but also in primary tumors. Here, MSI2 is linked to breast carcinoma.