CFTR and colorectal carcinoma: By using CRC-derived organoids and Air Liquid Interface (ALI) models, we focused on L1077P/L1077P homozygous, L1077P/W1282X and L1077P/R1066C compound heterozygous genotypes, characterizing the CFTR biochemical defects and their residual and pharmacologically rescued function in response to clinically approved CFTR modulators and their combinations, including the triple combination of TrikaftaTM-comprising drugs: Elexacaftor, Tezacaftor and Ivacaftor (ETI).