These results suggest that, in contrast with PID cases that carry STAT3 mutations, involvement of hematopoietic progenitor cells by STAT3 mutations is not a frequent finding in LGLL and, thereby, it does not explain the overall decreased production of hematopoietic cells observed in common in both diseases; alternatively, the presence of (over)proliferating STAT3 mutated LGLs in BM might indirectly impact on normal hematopoiesis, because of resource competition. This evidence concerns the gene STAT3 and pelvic inflammatory disease.