By contrast, treatment with the FDA‐approved pan‐HDAC inhibitor SAHA (vorinostat) was unable to efficiently abrogate HH/GLI signaling (Fig. 2f), which may be a consequence of targeting HDAC6, whose inhibition has been shown to promote ciliogenesis and HH signaling.14 Together, we conclude that 4SC‐202 represses HH/GLI signaling by blocking class I HDACs, in line with a recent report identifying HDAC1/2 as important positive effectors of HH/GLI signaling in a murine model of medulloblastoma.15 This evidence concerns the gene GLI1 and medulloblastoma.