A demonstration that anti-apoptotic members of the Bcl-2 family can modulate cell-death in this model came from experimental over-expression of Bcl-xL in β-cells via the rat insulin promoter (RIP-Bcl-xL), which resulted in suppressed apoptosis and an increase in tumor burden, along with a general “acceleration” of the tumor pathway [15]. This evidence concerns the gene BCL2L1 and neoplasm.