Findings from the present study, for instance, lower lamin b1 and higher p16Ink4 and IL-1β in deep endometriotic endometriosis, and a pro-inflammatory milieu in the lesions and eutopic endometrium, mediated by the SASP, suggest that a portion of deep endometriotic endometriosis cells might be entering the senescence state, which may explain some key characteristics of the disease. Here, IL1B is linked to endometriosis.