For example, studies with patient-derived organoids, xenografts, and lineage tracing have shown high plasticity in CRC, where tumors can persist after CSC ablation through reacquisition of stem-like traits independent of niche signals.180–182 Similarly, in lung adenocarcinoma, oncogenic signaling as elicited by KRAS proto-oncogene, GTPase (KRAS) mutations initiate lineage reprogramming by activating ERK signaling.183 Extrinsic factors, including microenvironmental cues and therapeutic stress, can also drive cellular plasticity. The gene discussed is KRAS; the disease is colorectal carcinoma.