The observed co-expression of Mcl-1 in circulating DEspR+citH3+[NET+Ns] aligns with the pathogenic hypothesis that as Mcl-1 underlies neutrophil extended survival [16], circulating DEspR+Mcl1+non-disrupted [NET+Ns] resist apoptosis-dependent clearance, thus contributing to the association of increased NETs with severity in RA. This evidence concerns the gene MCL1 and rheumatoid arthritis.