Table 2.

Summary of next-generation sequencing (NGS) studies.

Study	Tumor Type (n)	Genetic Alterations	Key Findings
Clark et al. (2013) [36]	WHO I/II (243/57)	NF2/ch22q loss TRAF7/KLF4 TRAF7/AKT1 SMO	Mutually exclusive non-NF2 driver mutations. NF2 tumors are more aggressive. Non-NF2 tumors are benign and localize to medial skull base.
Brastianos et al. (2013) [37]	WHO I/II/III (47/15/3)	NF2/ch22q loss SMO AKT1	As above.
Reuss et al. (2013) [38]	Secretory (30)	TRAF7/KLF4	All secretory meningiomas carried the KLF4 K409Q mutation.
Clark et al. (2016) [39]	WHO I/II/III/? (552/214/7/2)	POLR2A SMARCB1	Identification of POLR2A driver mutation. SMARCB1 and NF2 mutations co-occur.
Agnihotri et al. (2017) [40]	Radiation-induced (31)	NF2/ch22q loss	NF2 gene rearrangements common in radiation-induced tumors. Non-NF2 driver mutations not observed.
Bi et al. (2017) [41]	WHO I/II/III (75/113/21)	NF2/ch22q loss Genomic instability	NF2/ch22q loss and genomic disruptions occur early in progression and remain consistent over time.
Harmanci et al. (2017) [42]	WHO I/II/III/? (548/211/7/9)	NF2/genomic instability NF2/SMARCB1	NF2 is the sole driver mutation in atypical meningiomas and occurs in conjunction with genomic instability or SMARCB1 mutations.
Patel et al. (2019) [43]	WHO I/II/III (119/33/5)	Loss of PRC2 or DREAM complex repression	Transcriptional signatures identified a sole subgroup with recurring tumors, characterized by DREAM target genes activation.