High-throughput screening of a panel of targeted therapy agents CRC PDOs was done, and it was observed that TP53-mutation organoids were insensitive to nutlin-3a (MDM2/TP53 inhibitor), and KRAS-mutant organoids were resistant to the cetuximab and afatinib (the EGFR inhibitors) [22]. This evidence concerns the gene KRAS and colorectal carcinoma.