Genetic variations related to immune system function or response may influence individual susceptibility to meningiomas.[4,5] Furthermore, immune cells might contribute to the risk of meningioma initiation and progression by producing inflammatory mediators or causing tissue damage through inflammatory responses.[6–8] Similarly, during treatment, immune cells may release damage-associated molecular patterns, such as ATP and HMGB1, which stimulate the production of immune-stimulatory cytokines like IL-1α. This evidence concerns the gene IL1A and meningioma.