GALC and Krabbe disease: In addition, a late onset manifestation of GALC deficiency in Twi mice underwent massive gene therapy (galc transgene) consisting of brain lesions associated with leakage of the blood–brain barrier and plasma fibrinogen extravasation (PFE), with consequent activation of the fibrinogen-bone morphogenic protein (BMP)-SMAD-glial fibrillary acidic protein (GFAP) glia response [24].