HIF1A and colonic neoplasm: 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).