RhoA‐ROCK signaling has also been implicated in oxidative stress and neuroinflammation.[58, 59] Its aberrant activation aggravates neuroinflammatory responses, blood‐brain barrier disruption, neuronal apoptosis, and axonal damage, particularly after ischemic stroke.[60] Building on this foundation, our study provides evidence supporting the involvement of ARHGAP8‐mediated RhoB/C‐ROCK2 signaling in the regulation of actin cytoskeletal remodeling. The gene discussed is ARHGAP8; the disease is ischemic stroke.