These included 5 isogenic clonally-derived arachnoidal cell (AC-CRISPR) lines [11], of which two are merlin-wildtype controls (Syn1 and Syn2) and three are merlin-deficient lines generated by CRISPR/Cas9 NF2 inactivation (Syn3, Syn4, and Syn5), along with the immortalized merlin-deficient benign meningioma (MN) line Ben-Men-1 (Syn6) [12], as well as six patient-derived primary merlin-deficient MN lines (Syn7-Syn12). This evidence concerns the gene SYN3 and benign meningioma.