In transcriptional analyses of 11 pre-treatment and four cycle two tissue biopsy specimens, we identified suppression of JAK2-induced genes (SOCS3, EGFR) and STAT3 signatures, induction of JAK2-suppressed genes (including LCK), and JAK–STAT signaling as the top gene ontology in differential gene expression also consistent with a pharmacodynamic effect of ruxolitinib on tumor cells. The gene discussed is JAK2; the disease is neoplasm.