In a recently published article in Science, Zak et al. discovered that the Janus kinase (JAK) inhibitor ruxolitinib alters innate and adaptive immune cells to an unanticipated, predominantly immune-stimulatory phenotype in mouse infection models.1 This finding motivated a clinical study, which showed that ruxolitinib treatment in combination with the anti-PD1 immune checkpoint inhibitor (ICI) nivolumab in a cohort of relapsed or refractory Hodgkin lymphoma (HL) patients demonstrated promising responses. The gene discussed is PDCD1; the disease is Hodgkins lymphoma.