We note that during the initial stages of the work, to reduce the number of parameters in the model, we attempted to use a single concentration of c-Myc as the half-saturation constant for all regulatory interactions that promote cell survival (e.g. Bcl-2 upregulation, Mcl-1 upregulation, Bim inhibition), i.e. the onset of the cancer zone, as well as a single concentration for all regulatory interactions that promote apoptosis (e.g. Bcl-2 inhibition, Bax upregulation, Bak upregulation, Bim upregulation), i.e. the onset of the apoptosis zone, see Table A in S1 Text. The gene discussed is MYC; the disease is cancer.