CF is caused by a mutation in the gene cystic fibrosis transmembrane conductance regulator ( CFTR ). The most common mutation, ΔF508 , is a deletion ( Δ signifying deletion) of three nucleotides  that results in a loss of the amino acid phenylalanine (F) at the 508th position on the protein. This mutation accounts for two-thirds (66–70%  ) of CF cases worldwide and 90% of cases in the United States ; however, over 1500 other mutations can produce CF.  Although most people have two working copies (alleles) of the CFTR gene, only one is needed to prevent cystic fibrosis. CF develops when neither allele can produce a functional CFTR protein. Thus, CF is considered an autosomal recessive disease .
Limited data are available to help determine whether tocolytic therapy is indicated after preterm PROM. As described above, corticosteroids and antibiotics are beneficial when administered to patients with preterm PROM, but no studies of these therapies combined with tocolysis are available. Tocolytic therapy may prolong the latent period for a short time but do not appear to improve neonatal outcomes. 26 In the absence of data, it is not unreasonable to administer a short course of tocolysis after preterm PROM to allow initiation of antibiotics, corticosteroid administration, and maternal transport, 27 although this is controversial. Long-term tocolytic therapy in patients with PROM is not recommended; consideration of this should await further research.