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0 reviewsScarring is an insurmountable obstacle for axonal regeneration in recovery from spinal cord injury (SCI). It impedes the repair effectsof therapeutic targets in cortical neurons, such as PTEN−/− and hyper-IL-6, which cannot break through dense scar barriers toreconstruct neural circuits. However, methods for eliminating this process remain elusive. Here, we conducted a multiomics analysisof SCI and identified FBXL12 as an effective target for inhibiting scarring, further promoting spontaneous crossing of axons at theepicenter. We identified N6-Methyladenosine (m6A) modification as the predominant mRNA modification in SCI, with Fbxl12 beinga major modification target. Furthermore, m6A modification specifically promoted FBXL12 synthesis in activated microglia. Theoverexpression of FBXL12 in microglia contributed to its homogeneous distribution and maintained a “scar-less healing”phenotype. Remarkably, FBXL12 therapy effectively reduced extracellular matrix deposition and decreased the scar area by ~70%.Importantly, axons grew through the epicenter and reached a length of more than 2.4 mm 56 days post-SCI, significantly improving1234567890();,:motor function and reconstructing the neural circuit. Mechanistically, FBXL12 promoted cytoskeletal reorganization and migrationin microglia by catalyzing the K63-linked ubiquitylation of Myosin heavy chain 14 (MYH14). Together, our results identify m6AFBXL12-MYH14 axis as a novel cytoskeletal reorganization pathway in activated microglia and suggest FBXL12 as an effective targetfor a novel microglia-based approach to facilitate scarless functional recovery in SCI.Signal Transduction and Targeted Therapy (2025) 10:259 ;