Inhibition of Hh signalling using sonidegib in TP53-deficient allograft and xenograft models, or genetic inactivation of Smo in the Trp53 and Rb1 conditional genetic mouse osteosarcoma model, leads to tumour inhibition and osteosarcoma cell differentiation into mature bone, suggesting that Hh signalling acts to prevent terminal differentiation, enabling tumour growth [105]. Here, SMO is linked to neoplasm.