There has been an increasing number of studies contributing to the mechanistic understanding of aspirin’s anti-tumour effects in CRC including regulation of wingless-related integration site (Wnt), nuclear factor kappa light chain enhancer of activated B cells (NF-κB), hypoxia-inducible factor-1α (HIF-1α), mammalian target of rapamycin (mTOR), and phosphatidylinositol 3-kinase (PI3K) pathways which is the subject of excellent reviews (Figure 1) [20, 22, 39, 40]. The gene discussed is HIF1A; the disease is neoplasm.