In support of this notion, knockdown of Sam68, PARP1, and p65 in human colon cancer cells significantly reduces the basal and genotoxic stress-induced PAR production, NF-κB activation, and expression of anti-apoptotic molecules Bcl-XL and XIAP, thus leading to spontaneous and DNA damage-induced apoptosis in Sam68-downregulated colon cancer cells. The gene discussed is BCL2L1; the disease is colonic neoplasm.