p. administration) inhibited tumor growth in allograft models of MB derived from both SmoWT and Smo resistant-mutant SmoD477G; Ptch+/-; Trp53−/− mice, as consequence of the downregulation of Gli1 gene expression (>50% compared to PLGA-PEG NPs used as control) (Chenna et al., 2012). The gene discussed is PTCH1; the disease is neoplasm.