Notably, we also found that p16-positive regions of meningiomas with CDKN2A deletion still demonstrated the same CDKN2A loss detected in the bulk tumor, suggesting either a lack of specificity of p16 IHC or the nature of CDKN2A loss as a late, subclonal event in tumorigenesis. The gene discussed is CDKN2A; the disease is neoplasm.