In addition to the consistent demonstration of CTLA-4 and PD-1 participation in the immunosuppression associated with the severe forms of human and experimental PCM (17, 18, 20–24), the successful use of checkpoint inhibitors for the control of neoplasms (34) and some fungal infections (6, 7) led us to postulate that the inhibition of these molecules could have a beneficial effect on PCM. The gene discussed is PDCD1; the disease is fungal infectious disease.