A working model for redox regulation of T-cell turnover by p13. Data in the present study revealed a gradient of ROS in primary versus transformed T cells, with very low levels in resting cells, higher levels in stimulated cells, and substantially higher levels in transformed Jurkat cells. By increasing mitochondrial ROS production, p13 favors activation of primary resting T cells while promoting death of transformed T cells. These findings suggest that p13 may have a distinct impact on cell turnover depending on the inherent ROS levels, and that in the context of the HTLV-1 propagation strategy, p13 could increase the pool of “normal” infected cells while culling transformed T cells, thus favoring lifelong persistence of the virus in the host.