Our model was not compatible with the dynamics of PDCD1/CD274 as sole correlates of the exhausted state, which appears at first sight to contradict reports indicating that PDCD1/CD274 signaling is relevant for immunosuppression in melanoma,31,32 although our result agrees with others showing that B16F10 in particular may be resistant to PDCD1 antagonist monotherapy.33 This evidence concerns the gene PDCD1 and melanoma.