These findings altogether suggest an intricate interplay of HH/GLI signaling and pro-inflammatory effectors generating a tumor-promoting environment and it will be pivotal to decipher these reciprocal interactions in a cancer entity- and context-dependent manner for the development of future combination therapies interfering with HH/GLI itself together with cooperative pro-inflammatory pathways (Fig. 2). This evidence concerns the gene GLI1 and neoplasm.