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). This evidence concerns the gene HIPK2 and neoplasm.