Although we did not detect sustained Stat3 mRNA elevation—likely due to negative feedback by SOCS3 (Gao et al., 2018)—the persistent Il6 mRNA overexpression suggests that post-transcriptional activation of STAT3 or alternative pathways (e.g. MAPK) may underlie lesion progression in adenomyosis. Here, STAT3 is linked to adenomyosis.