Among them, STAT5 is the most critical regulator of cell proliferation and survival,46,47 while STAT3 is essential for pro-inflammatory cytokine production; indeed, pan-hematopoietic STAT3 deletion remarkably attenuated cytokine secretion in an MPN mouse model.48 Here, we observed dose-dependent inhibition of both STAT3 and STAT5 phosphorylation following MCL treatment, which probably plays an important role in the anti-inflammatory and anti-tumor effects elicited by MCL. The gene discussed is STAT5A; the disease is myeloproliferative disorder.