Other research looked at the role of the FPR1 gene using a microfluidic device where immune cell migration towards and interaction with chemotherapy treated cancer cells could be recorded.40 This model was subsequently modified to study PBMC recruitment towards ECM-embedded (Matrigel) cancer cells exposed to decitabine (DAC) and/or IFN.42 Greater infiltration of PBMC was reported toward tumour cells treated with both DAC and IFN in comparison to one agent alone and to untreated cells. The gene discussed is FPR1; the disease is cancer.