The differences observed in the cell lines in response to CGA treatment, being SW480 more susceptible than HT-29 cells (Figure 3, Figure 4 and Figure 5), could be explained by its genetic and epigenetic backgrounds, which have a direct impact on the constitutive activation of signaling pathways involved in colon cancer onset and progression, such as TP53, KRAS, BRAF, Wnt/β-catenin, among others [78,79]. The gene discussed is KRAS; the disease is colonic neoplasm.