Mechanistically, these vascular and matrix signals cross with mTOR-centered stress and growth pathways: in vascular systems, modulation of mTOR activity influences endothelial inflammatory tone, growth/repair programs, and angiogenic gene expression, providing a route by which lesion-level angiogenesis and ECM turnover can strengthen neuroinflammatory and metabolic shifts in FCD [138]. The gene discussed is MTOR; the disease is fleck corneal dystrophy.