The fact that this phenomenon was observed with both CRISPR strategies (i.e., correction of the V600E mutation in colon cancer organoids and knock-in of the V600E mutation of healthy colon organoids from the same patient), suggests a key role for BRAFV600E in gene body hypermethylation of TCF4, leading to activation of WNT signaling in colon cancer. The gene discussed is TCF4; the disease is colonic neoplasm.