CHI3L1 and endothelial dysfunction: Chi3l1 may play an important role in the pathogenesis of OSAS by increasing the proliferation of tonsil lymphocytes via the ERK1/2 pathway and causing endothelial dysfunction via VEGF signaling, thereby potentially triggering or exacerbating many serious complications, such as hypertension and liver fibrosis in patients with OSAS (Figure 2) [59,60,61,62].