Our CNV analysis found the amplification of Cylin E1 (CCNE1) in response to dabrafenib-induced resistance in 3D-HT-29 spheroids, which was corroborated by previous studies where CCNE1 amplification was detected in most of the solid cancers, including CRC [50], suggesting CDK2 inhibitors can be used as potential second-line agents to reverse dabrafenib resistance in our system [72]. The gene discussed is CDK2; the disease is colorectal carcinoma.