Patients with AML aged over 60 may have an increased risk of second primary malignancies, including CRC [43]; therapy-related AML (t-AML) can occur in CRC patients as a direct consequence of mutations induced by various anticancer therapies, such as chemotherapy and radiation therapy [44]; Sawa-Wejksza et al., has demonstrated that, although CRC-CM inhibited proliferation of THP-1 AML cells, it increased expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 9 (MMP-9) THP-1 cells, key inducers of angiogenesis and metastasis, respectively [22]. The gene discussed is VEGFA; the disease is acute myeloid leukemia.