The ability of kinetin to correct the splicing of CFTR in vitro was verified, and the effect of kinetin on CFTR splicing in cultured epithelial cells from nasal brushing of 3 CF patients and in 3 lymphoblastoid lines has been tested and confirmed; in particular, researchers verified that the treatment is capable of increasing wild-type mRNA. Moreover, they tested the efficacy of 8 additional compounds among which RECTAS proved to be the best, being active at a concentration ∼10 fold lower than kinetin, confirming that kinetin impacts on the expression of a limited number of genes. Other results of the projects include producing a dual-fluorescence reporter vector for the validation of lead compounds and confirming that the mechanism of action of kinetin on CFTR splicing does not depend on specific in-cis sequence elements reported for other genes and may be mediated by the level of the splicing regulatory protein hnRNPA2B1.