The causal relationships between caspase-3/EndoG and Src activation was further confirmed through immunohistochemistry staining of tumor samples from caspase-3- or EndoG-deficient xenografts, which indicated the downregulation of phosphorylated Tyr416 Src expression, and upregulation the non-phosphorylated Tyr416 Src expression in caspase-3- or EndoG-deficient tumors (Fig. 5D, E). The gene discussed is SRC; the disease is neoplasm.