For example, the LEF1-inclusion isoform could promote cell proliferation and maintenance of B cell identity—as observed in the C/EBPα-dependent transdifferentiation system and in pancreatic cancer cell lines [66, 67], while gradual skipping of exon 6 might alter its effect on its target genes with the consequence of inducing pluripotency, most probably in a β-catenin-independent way. The gene discussed is LEF1; the disease is pancreatic neoplasm.