Previously, we have shown that sustained c-Myc inactivation in locally invasive pancreatic islet tumours (induced by c-Myc activation in β-cells on a background of Bcl-xL overexpression) induced β-cell growth arrest and re-differentiation into mature β-cells, accompanied by the collapse of tumour vasculature and tumour cell mass resulting from apoptosis, despite the constitutive expression of Bcl-xL in the tumour cells [9]. Here, BCL2L1 is linked to neoplasm.