NOTCH signalling is a essential for development and the regulation of self-renewing tissues. Aberrant activation of the NOTCH pathway leads to deregulation of a range of cellular functions which ultimately drives oncogenic transformation (
e.g. sustained proliferation, evasion of cell death, loss of differentiation capacity, invasion and metastasis) [
1]. Inhibition of NOTCH pathway signalling has therefore emerged as a novel mechanism for therapeutic intervention in NOTCH-driven cancers [
2]. A number of strategies have been developed that target NOTCH siganalling at different levels of the pathway; for example monoclonal antibodies that block the function of NOTCH ligands (
e.g.
demcizumab) or NOTCH receptors (
e.g. tarextumab), small molecule γ-secretase inhibitors (
e.g.
PF-3084014) and inhibitors that block formation of the nuclear NOTCH transcriptional activation complex (
e.g. CB-103).