Specifically, studies have looked at the biochemical and cellular level to understand the pathophysiology behind LC, such as dysfunction in clotting proteins and the lytic system leading to hyperactivated platelets and circulating micro-clots [12], and persistence of a cytotoxic program evident in CD8+ T cells with elevated production of type 1 cytokines and interleukin-17 (IL-17) [13]. Here, CD8A is linked to laryngotracheoesophageal cleft.