Ruxolitinib’s potent inhibition of CXCL10 production is an important finding because this chemokine recruits Th1 cells via the cognate receptor CXCR3 and thus contributes significantly to Th1-high asthma and failure to respond to corticosteroids (Gauthier et al., 2017). The gene discussed is CXCL10; the disease is asthma.