TGFB1 and glioblastoma: Interestingly, SMAD proteins are activated in a TGF‐B‐dependent manner [64], and some of the heterogeneity of GBM subtypes may be explained by particular post‐translational modifications, such as phosphorylation and palmytoilation [65, 66], which modify SMAD3 activity and may promote the transcriptional rewiring that leads to a MS‐like phenotype.