As subset-specific distinction of neutrophils is key to therapeutically modulating pathogenic neutrophils while sparing homeostatic neutrophil subtypes, we tested the hypothesis that long-lived, pro-injury DEspR+neutrophils capable of NET-formation in the circulation in sterile inflammation are present in RA patients during clinical exacerbation or RA flare, despite pro-neutropenia RA maintenance therapy. Here, FBXW7-AS1 is linked to neutropenia.