On the whole, the results of the present study allow us to affirm that treatment with a dual inhibitor of GSK3β and PDE7 in a “primary-progressive” preclinic MS model is capable of (i) modulating the inflammatory response, (ii) influencing neuroprotective mechanisms and (iii) promoting the differentiation of OPCs, to achieve greater preservation of myelin and axonal integrity. This evidence concerns the gene GSK3B and myeloid sarcoma.