MAIT cells are readily activated during human infection, via both TCR dependent and independent mechanisms. Previously we have addressed how these different triggers drive different functional outcomes for the cells. In this talk I will update further on this, using a more time-resolved approach and exploring the role of individual transcriptional modules. I will explore a model where divergent functional outcomes can be obtained from the same basic MAIT cell by integration of TCR signals and cytokine signals over time and the implications for this in vivo.