CFTR and cystic fibrosis: Further studies demonstrated the feasibility of this approach for correcting: (a) the CCR5-Δ32 mutation, involved in HIV-resistance [133,146] in different in vitro and in vivo investigations [143,147], over-performing the selectivity of other nuclease-based agents known at the time [148]; (b) the defective cystic fibrosis transmembrane conductance regulator (CFTR) [149], using vehicles coated with a synthetic CPP called MPG [120] on a model system bearing defective a EGFP fusion gene [113], and subsequently for the correction of the real CFTR gene both in vitro and in CF mice [150].