Candida parapsilosis is an important fungal pathogen that is particularly isolated from blood cultures. In recent years, although there are regional differences between centres, resistance to fluconazole which is the most commonly preferred drug for candidemia, has increased in many regions. This increase complicates infection control and adversely affects treatment. In C.parapsilosis, codon 132 Y/F change in ERG11 is accepted as the dominant mechanism and it is reported that some amino acid changes in MRR1 may also contribute to resistance. In this study, we aimed to elucidate the azole resistance mechanisms of ERG11 and MRR1 in C.parapsilosis sensu stricto isolated in our centre. 30 C.parapsilosis sensu stricto obtained from patients with candidemia in 2018 and 2019 were tested for susceptibility to fluconazole by broth microdilution method and amplified by colony polymerase chain reaction approach and DNA sequence analysis was performed on selected regions. As a result of the analysis, Y132F mutation was identified in one susceptible isolate while Y132F, G307A and K143R mutations were detected in resistant isolates in ERG11; R405K mutation was detected in one susceptible isolate whereas G927C mutation was observed in the resistant isolates in MRR1.R398I mutation in ERG11 was detected in dose-dependent susceptible and sensitive isolates. Although Y132F mutation is the primary mechanism and the most frequently detected mutation, potential mechanisms should not be neglected. In our study, the G307A and G927C mutations detected in resistant isolates were observed as single mutations in some of the samples. Similarly, the R398I mutation in susceptible isolates was identified alone. Studies aimed at elucidating these mechanisms will contribute to the proper development of therapeutic strategies.