To determine if miR-206 contributes to the pathogenesis of RMS in vivo, we utilized miR-206 loss of function mice17 in a previously described mouse model of FN-RMS.32 We bred miR-206+/−; SmoM2/M2 to aP2-Cre; miR-206+/− mice to compare tumor onset kinetics in littermate miR-206+/+ wild type (WT), miR-206+/− heterozygous (Het) and miR-206−/− homozygous null (KO) mice that are also aP2-Cre; SmoM2/+ (Supplementary Figure S9a). This evidence concerns the gene FN1 and neoplasm.