Therefore, to investigate whether the homozygous form of FH with hypercholesterolemia influenced the severity of IS, we also performed c-MCAO on homozygous LDLR KO hamsters and found that unlike heterozygous FH in hamsters, homozygous FH showed a significant increase in infarct volume and BBB disruption accompanied by a local inflammatory response, indicating that one copy of the Ldlr gene may be sufficient to confer protection against IS, whereas a total loss of the Ldlr gene exacerbates IS. The gene discussed is LDLR; the disease is familial hyperaldosteronism.