In the nucleus, MRTF acts as a positive transcription cofactor for GLI1, sharing chromosomal occupancy with GLI1, thus amplifying GLI1 transcriptional activity in resistant BCC.[52] Additionally, the loss of primary cilia confers protection to tumor cells against Smo inhibitors, as it sustains GLI2 activity in resistant medulloblastoma cells.[53] Our findings indicate that OSCC cells lack primary cilia, which diminish with increasing substrate stiffness (Figure S3, Supporting Information). Here, GLI1 is linked to neoplasm.