We suggest that the cause of these cases may have to do more with antigen processing (and presence) and its combined effect within the tumor microenvironment than with just the physiological parameters represented in the simulations thus far that did not focus on variations in mAPC activation, antigen abundance per cell and tumor chemokine levels, as well as different combination of CD80, PD1, PDL1 and PDL2 expressed on the cancer cells. This evidence concerns the gene PDCD1LG2 and cancer.