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Additionally, the S/T-3A mutation 37 , which disables serine/threonine phosphorylation sites at residues 356, 361 and 375 of XKR8, but not the 2DA mutants, enabled XKR8 KO HL-60 cells to expose PS in response to apoptosis induced by doxorubicin and NET induction by PMA, thereby restored the NET formation (Fig