Upon activation by stimuli such as reactive oxygen species (ROS), it leads to the cleavage of caspase-1 and subsequent secretion of the mature forms of the proinflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), which can promote neuronal death in glaucoma, along with other neurodegenerative diseases [32–36]. This evidence concerns the gene IL1B and glaucoma.