The effect of BCL3 suppression on a selection of canonical and stem-cell specific WNT target genes demonstrated the downregulation of LGR5 and ASCL2 expression, whereas the canonical WNT targets remained unaffected [13] suggesting that BCL3 acts as a context dependent modulator of β-catenin/TCF-mediated transcription, potentially restricted to stem-like tumour cells. The gene discussed is BCL3; the disease is neoplasm.