Though the above-mentioned experimentally established model based on a triggering function of CAP and PAM-derived H2O2/nitrite sufficiently explains selective cell death in tumour cells, also based on their own RONS [42], surprisingly a recently published mathematical model [45] claimed that catalase-dependent activation of the apoptotic/cell death pathways is unlikely to contribute to the observed anti-cancer effect of CAP. The gene discussed is CAT; the disease is neoplasm.