Our study identified that ESC-derived PGI2 contributed to CD16− NK-cell differentiation in a PTGIR-dependent manner and that the CD16− NK-cell subpopulation promoted EMs progression in vivo, which reinforced the widely accepted hypothesis that CD16− NK cells possess a strengthened regulatory function and weakened killing activity; thus, the approach of hindering CD16− NK-cell accumulation in the peritoneal cavity of EMs patients might be considered an immune-based therapy for combating EMs. Here, PTGIR is linked to eosinophilia-myalgia syndrome.