The conversion from healthy human intestinal organoids to colorectal progressive tumoroids has been achieved through the introduction of a set of common driver mutations in colorectal cancer via CRISPR-Cas9 gene editing technology, indicating tumor growth as a consequence of cancer driver mutations was independent of SC niche factors and identifying loss of adenomatosis polyposis coli (APC) and TP53 as pivotal contributors for chromosome instability and aneuploidy [24, 90]. The gene discussed is TP53; the disease is colorectal cancer.