To determine the effect of mir-17~92 loss on pancreatic development, we induced pancreas-specific deletion of the mir-17~92 cluster using the conditional mir-17~92flox allele and the recombination driver Ptf1a-Cre [40, 41]. qRT-PCR of RNA from whole pancreata showed a strong reduction in the levels of mir-17~92 constituent miRNAs in compound mir-17~92flox/flox, Ptf1a-Cre mice (Supplementary Figure 2A). The observed residual mir-17~92 expression is likely from endocrine cells, many of which are derived from a PTF1A-independent lineage [40, 42], as well as a small population of acinar and ductal cells that have avoided recombination due to the fact that Cre drivers are not 100% efficient . Expression from the paralogous mir-106b~25 cluster is unaffected (Supplementary Figure 2A). Despite efficient depletion of mir-17~92 miRNAs from the pancreas, organ size and exocrine and endocrine architecture and composition were unperturbed (Supplementary Figure 2B). These findings demonstrate that mir-17~92 is not required for normal pancreas development.