The 3272-26AàG cystic fibrosis (CF) mutation creates an alternative splicing site on intron 17a which competes with the normal site, causing a frameshift and premature stop codon. The investigation’s purpose was to construct a successful diagnostic assay for the mutation’s presence. We hypothesized an 800 base pair band since primers 1 and 2 will anneal to DNA if mutation is present (Beck et al, 1999). PCR with three primers directed the synthesis of a targeted region of template DNA followed by gel electrophoresis (Wright et al, 2009). PCR yielded presence of mutation in Mutant DNA and absence in Wild-type DNA. Mutation is significant since one 3272-26A>G allele, heterozygous with severe ΔF508 allele, results in significant reduction of phenotypic severity, and it is plausible that two 3272-26A>G alleles would avoid CF completely (Amaral et al, 2001). The purpose of independent research was to examine CF on a personal level to compliment molecular level research in determining correlation between CF severity and health-related quality of life (HRQOL) for effective CF management. We hypothesized CF reduces HRQOL in afflicted patients based on severity of disease which relates to risk factors and cost.  Through internet research and analysis, increased severity was found to be classified with increased risk factors which had various effects upon HRQOL. Research is significant in tailoring patients’ treatment by using risk factors to develop strategies to increase HRQOL, where screening and genetic counseling is encouraged. In conclusion, assay was successful and HRQOL problems less severe in this mild 3272-26AàG mutation.