SMO and neoplasm: This pathway is initiated by binding tumor cell-derived Hh ligands to patched 1 (Ptch 1) receptor in CAFs membrane, subsequently, the inhibition of smoothened (SMO) protein is relieved, which triggers activation of the glioma-associated oncogene transcription factor (Gli1-2), leading to downstream genes expression and abundant ECM production (Zhang et al., 2018).