Additionally, it was demonstrated that silencing the GLI-1 protein decreases the expression of GLI1-AS, while overexpression of GLI-1 increases GLI1-AS, supporting the hypothesis of a negative/positive biofeedback loop where GLI1-AS is the genetic target of the transcriptional factor GLI-1 at the protein level; this epigenetic-transcriptional relationship contributes to the biomedical and clinical impact of the Hh pathway in the progression of human carcinomas [115]. Here, GLI1 is linked to carcinoma.