This process involves tumor cell cycle arrest, accompanied by a decrease in the expression of cyclin A and cyclin-dependent kinase-2 (CDK2) (Maurya et al., 2010; Ma et al., 2012; Magatti et al., 2012; Wu et al., 2013), and/or promotion of tumor cell apoptosis, with upregulation of apoptotic genes (caspase-3 and caspase-9), and downregulation of anti-apoptotic genes [survivin and X-linked inhibitor of apoptosis protein (XIAP)] (Wu et al., 2013). The gene discussed is XIAP; the disease is neoplasm.