TGFB1 and neoplasm: Converting specific CAF subtypes into a less activated state or shifting tumor-promoting CAF subtypes toward a quiescent or tumor-restraining phenotype—or even neutralizing ligands that activate fibroblasts into specific CAF subtypes such (e.g., IL-1, IL-6, LIF, and/or TGF-β)—may open up completely new druggable pathways [82], which is potentially important in OSCC where iCAFs have been shown to have a potential crucial role [25,63,64,66,67].