Specifically, MAPK15 down-regulation diminished the HH transcriptional response when the pathway was stimulated, in NIH3T3 cells, with the agonist SAG, acting on the endogenous G protein-coupled receptor (GPCR) SMO, but also in DAOY and ONS-76 MB cells, both representing typical models for investigating the effect of canonical HH signaling in tumor development. The gene discussed is SMO; the disease is neoplasm.