As the MCAO-KM or MCAO-LM in rats, similar to the respective MCAO models in mice, are presently used randomly, and, most importantly, the data are compared without taking into account the specific features of each model, we have recently studied the early post-stroke period in the MCAO-KM and MCAO-LM in rats and found that, though the infarct volumes and neurological deficits were similar in both models, the MCAO-KM rats demonstrated a greater secretion and accumulation in the hippocampus and FC of corticosterone and IL1β [15]. Here, IL1B is linked to stroke disorder.