While it does not induce Th17 differentiation or IL-17A production from naïve CD4+ T cells on its own—due to the absence of substantial IL-23 receptor (IL-23R) expression—IL-23 plays a crucial role in sustaining the pro-inflammatory Th17 axis, contributing to ongoing immune activation in PV [81,82], this finding supports the important role of Th17 cells in the pathology of MPNs. The gene discussed is IL23R; the disease is acquired polycythemia vera.