Importantly, we show that this upregulation of stromal Shh expression is dependent on the presence of a mixed population of both αSMA+ and αSMA− cells in which periostin is also upregulated, and mesenchymal cell growth is accelerated, thus further supporting the concept of the formation of a mesenchymal niche, with a phenotype different from that of either of the αSMA+ or αSMA− cells alone, that could contribute to pancreatic cancer progression. Here, ACTA1 is linked to familial pancreatic carcinoma.