Abnormal activation of the interleukin (IL)-36-chemokine-neutrophil axis, dysregulation of innate immune responses, and ensuing excessive neutrophil infiltration are implicated in the pathogenesis of GPP (18); whereas, PV is an autoimmune disease characterized predominantly by IL-23/17 signaling and self-sustaining inflammatory cycles [positive feed-forward inflammatory response (19)] that lead to disordered proliferation and abnormal differentiation of keratinocytes (20). This evidence concerns the gene IL37 and acquired polycythemia vera.