The fact that shRNA-mediated depletion of p53 is nearly complete in the cytoplasm of these cells (Figure 6d) suggests that measures capable of alleviating mutant p53 expression elicit the release c-Abl from the cytoplasm, thereby enabling this PTK to execute its anti-tumor activities and stabilization of wild-type p53 expression in the nucleus.27 In support of this, we asked whether the increase in nuclear c-Abl expression after Imatinib treatment correlated with an increase in its nuclear kinase activity. The gene discussed is TP53; the disease is neoplasm.