These markers correlate with the total volume of CMBs.29 Recent experimental advancements suggest that the deletion of myosin light chain kinase (MLCK) confers protection against CMBs and the cerebral effects of chronic dietary neuroinflammation, such as hyperhomocysteinemia.93 This discovery indicates that MLCK inhibition may represent a novel therapeutic avenue for combating tissue barrier dysfunctions, especially blood–brain barrier compromises, and could provide benefits in neuroinflammation-related models of vascular cognitive impairment and dementia.94 The gene discussed is MYLK; the disease is dementia.