Interestingly, given its role as a key tumor-suppressor protein regulating cellular apoptosis in response to cyto or genotoxic insults, we did not observe a statistically significant increase in p53 phosphorylated at Serine 15 (a site closely associated with DNA-damage response [44]), nor did we see an increase in the activation of either of the cell-cycle checkpoint proteins, Chk1 or Chk2. The gene discussed is CHEK2; the disease is neoplasm.