However, this might be explained by the hypothesis that AT/RT-SHH tumors rely on downstream activation of SHH signaling and, therefore, are independent of primary cilia for constitutive active SHH signaling as previously shown for the dual and opposing role for primary cilia in SHH-dependent medulloblastoma and basal cell carcinoma [22, 32], depending on the initiating oncogenic event. This evidence concerns the gene SHH and medulloblastoma.