In parallel to the autocrine/paracrine signaling modality of different proinvasive and angiogenic factors and inflammatory cytokines and chemokines, the formation of the p53/YAP/HIF-1α communication node is of particular interest because its activation depends on the ET-1 signal route, and in a self-magnifying circuit, in both tumor cells and stromal elements, this ultimately sustains escape from PARPi and unfavorable outcomes. This evidence concerns the gene HIF1A and neoplasm.