On the other hand, since the interaction between neuronal CD47 and microglial SIRP-α results in the inhibition of microglia [50], the inefficient CD47/SIRP-α interaction between misshapen cells and microglia within the epileptogenic lesions may conduce to microglial activation, which abundantly occurs in epileptogenic lesions of FCD IIb and TSC and is thought to perpetuate and prolong the inflammation [41, 51–53]. The gene discussed is CD47; the disease is tuberous sclerosis.