The researchers measured the actual amount of full-length CFTR mRNA using next-generation sequencing technologies (Nanopore and PacBio) capable of providing the sequence of long nucleic acid molecules (RNA or DNA). This analysis was carried out on samples of different tissues from CF persons (lung, testis, vas deferens, colon and pancreas) and in CaCo2 cells (human intestinal epithelium cell lines used as a model of the intestinal barrier). The project allowed to evaluate the effect of pharmacological intervention with kinetin and its derivative RECTAS, confirming their ability to correct the splicing in model cells CaCo2 and CuFi-1 (bronchial epithelial cell line derived from a person with fibrosis cystic homozygous for the Delta F508 mutation). Researchers characterized the mechanism of action of kinetin/RECTAS confirming a low level of off-target splicing modulation. The researchers would demonstrate the action of kinetin and RECTAS on further disease models (such as intestinal organoids) and they would also evaluate the amplifier effect of kinetin/RECTAS on CFTR protein.