Aiming to decipher the mechanism for the anti-angiogenic activity of hypericin [13], we examined whether hypericin affects HIF-1α adaptive stabilization, which occurs under hypoxia in the absence of proline and asparagine hydroxylation [1] in three human cell lines: U87-MG glioblastoma cells, RCC-C2VHL−/− (C2VHL−/−) renal carcinoma cells deficient in pVHL, and ARPE-19 retinal pigment epithelial cells. Here, HIF1A is linked to glioblastoma.