One such network (Additional file 2: Figure S1), which is activated on day 12 and may contribute to the early anti-tumor actions of CPA, includes many intracellular cell death factors, such as BIK, important for mitochondrial rupture, death effector signaling caspases, DNA repair and cell death signaling poly-A ribose polymerases (PARP10 and PARP12), tumor necrosis factor TNFSF10, the 20S proteasome, and several cytokeratins, including KRT18, which is released from CPA-treated tumors and is a biomarker for clinical response to therapy [36]. This evidence concerns the gene PARP12 and neoplasm.