TurboSPI has the potential to offer quantitative cell tracking with high fidelity R2* mapping. However, early in vivo studies demonstrated that accuracy of the R2* fitting deteriorates in the presence of off-resonance fat signal. In this work, we investigate these findings further with an in vitro study. We used in silico and in vitro data to develop and test a more comprehensive decay model that accounts for fat oscillations in the TurboSPI signal. The proposed model results in improved R2* estimates in the presence of fat.