The second hypothesis, that, as reflected by the identified modulations of Cobl levels acutely following ischemia and during stroke recovery, the actin nucleator Cobl may be a crucial player in the repair of the stroke-induced dendritic arbor defects in the penumbra within the observed narrow time window between day 1 and day 4 after MCAO was addressed by subjecting Cobl KO mice [37] to comparative and time-resolved MCAO studies evaluating the different dendritic parameters in a fully blinded manner. The gene discussed is COBL; the disease is ischemia.