Such cells would effectively only experience the inhibitory activity of ruxolitinib alone, which was shown previously to be rendered ineffective by compensatory BTK/NFκB‐mediated signaling pathways.5, 10 JAK2002 and JAK2003 who experienced disease progression on ruxolitinib (Table 2) had developed increased adenopathy on ibrutinib and would likely not have derived any benefit from simultaneous blockade of BTK/NFκB and JAK/STAT signaling pathways. This evidence concerns the gene BTK and lymphatic system disorder.