Since stromal HIF-1α expression in fibroblasts was detected in a very low proportion of PDAC patients, and positive correlation was revealed between stromal CAIX positivity and CAIX+ cancer cell areas (predominantly upregulated via HIF-1) [25], we can expect an additional regulatory mechanism (e.g., paracrine stimulation of CAIX expression in stromal cells), which is mediated via hypoxia-induced HH signaling from adjacent tumor cells. The gene discussed is HIF1A; the disease is neoplasm.