There has been a long-standing interest in the ocular inflammation that occurs in the acute and chronic stages of Stevens-Johnson syndrome (SJS) as well as toxic epidermal necrolysis (TEN). Several different causes of delayed ocular disease such as SJS- ocular surface failure (SJS‐OSF), SJS- recurrent inflammation (SJS‐RI), SJS- Scleritis (SJS‐S), and SJS- mucous membrane pemphigoid (SJS‐MMP) occurring in its natural course following the acute episode have been alluded to in earlier studies [1]. A collective understanding of the natural history of the disease and the windows of opportunity it presents at varying stages has undergone a paradigm shift over the years. Today we appreciate that the gradual ocular surface failure (OSF) and recurrent inflammation (RI) that occur in these eyes, could be largely attributed to what is referred to as mechanical causes for inflammation that have not been addressed. These include dry eye, lid margin keratinization (LMK), and adnexal disorders that contribute to continued blink-related micro-trauma and inflammation. Presently we understand that addressing these causes for mechanical inflammation can largely stabilize the ocular surface and prevent its complete failure as well as quell the episodes of recurrent inflammation. This explains the need to revise the earlier labeled SJS-RI and SJS-OSF. SJS-MMP, on the other hand, is associated with progressive cicatrization and needs to be managed accordingly. However, there exists a small subset of patients who continue to remain inflamed following the acute episode or develop severe inflammation in the chronic stage. These patients have either undergone surface stabilization procedures addressing the mechanical causes of inflammation or do not exhibit them at all. These patients represent a smaller, but distinctly different cohort of what has been described in the literature as SJS-RI and probably SJS-S, whom, we henceforth refer to as SJS- clinical non-responders (SJS-NR). The etiopathogenesis for this non-responsiveness in the chronic stage of SJS remains unclear. The primary objective of this study is to describe this subset of non-responders. The second objective is to examine the probable causes for this differential manifestation in these non-responders. Therefore, the tear samples from non-responders were analyzed to study the cytokine expression patterns in order to define biomarkers that might help in the early identification of non-responders.