To investigate whether loss of RASGAPs enables EGF-independent tumor cell growth and survival in CRCs, we depleted the activity of each RASGAP separately in P18T organoids using CRISPR-induced knock outs by targeting Cas9 cleavage activity against the conserved arginine finger in the catalytic GAP domain (Figure 2B) [53, 54]. This evidence concerns the gene EGF and neoplasm.