There is abundant evidence that survival factors can use the ERK1/2 pathway to increase the expression of several pro-survival Bcl-2 proteins, notably Bcl-2, Bcl-xL, and Mcl-1, by promoting de novo gene expression in a variety of cell types, for example, MEK inhibition caused a decrease in Bcl-2, Bcl-xL, and Mcl-1 and apoptosis in pancreatic cancer cells [20]. This evidence concerns the gene MCL1 and pancreatic neoplasm.