Because HSP90 bound and stabilized PKD2 in cancer cells, inhibition of HSP90 led to degradation of PKD2, thereby indirectly impacting the proangiogenic function of PKD2 under hypoxic conditions by blocking HIF1α accumulation and NF-κB/VEGF-A signaling activity [44,45]. The gene discussed is NFKB1; the disease is cancer.