Despite the established role of TLR in gliomas, three key mechanistic gaps remain unaddressed: (i) The differential expression patterns of TLR2/4 across glioma grades remain poorly characterized; (ii) The functional consequences of TLR signaling in grade-specific contexts are unclear; and (iii) The potential of TLR expression profiles to distinguish tumor-associated neuroinflammation from non-tumor conditions, such as epilepsy, needs further investigation. Here, TLR2 is linked to epilepsy.