Our previous study showed that knock-in (KI) of an Mcl-1 phosphorylation site mutant (S121A/E125A/S159A/T163A) in regorafenib-sensitive HCT116 CRC cells (Figure S1A) blocks regorafenib-induced Mcl-1 degradation and subsequent apoptotic response 9. This evidence concerns the gene MCL1 and colorectal carcinoma.