Recent in vitro and ex vivo studies have demonstrated a strong positive correlation between Galectin-3 expression and NLRP3, ASC, caspase-1, and IL-1β levels in OLP lesions, suggesting that Galectin-3 may serve as an upstream regulator of NLRP3 inflammasome activation during OLP progression [71]. This evidence concerns the gene NLRP3 and oral lichen planus.