HIF-1α is mostly regulated at posttranscriptional levels by low oxygen conditions [129]; however, the regulation by HIPK2 at the transcriptional level [85] suggests that inhibition of HIPK2 can induce a pseudo-hypoxic phenotype with HIF-1 activation and an “angiogenic switch”, leading to tumor progression, invasion, angiogenesis and resistance to therapies, that can be applied to colon cancer and also to other solid cancers (Figure 3). The gene discussed is HIF1A; the disease is neoplasm.