Mark Poznansky began his presentation very informally, as a conversation really- evocatively telling us about the origins of his research and also remembering key mentors, one of whom was his mother, a pathologist, Dulcie Coleman who alerted him to her cell culture work and her discovery with her colleagues of BK virus. He described how he had been fascinated to see how the thymus, with its matrix of stroma, harbors a population of differentiating cells, maybe it would not be immunologically inaccurate to think of them of cells undergoing their education, that would then- in a precisely timed way, leave the gland. He also recalled how impressed he had been as he entered this field by how readily thymocytes spill out from an isolated thymus gland when it is extirpated and gently squeezed. Clearly, there is not a durable barrier to their exit, so the in vivo process must be developmental biology. From these insightful and intimate recollections as his point of departure, Mark then described ingenious studies using chemokine gradients in microfluidic chambers that resulted in a major discovery, that certain leukocytes, including T cells and neutrophils can reverse their chemotactic behavior – a process he termed fugetaxis (from the Latin root, fugere). One is reminded of the scene in the movie “Fargo” when the car dealer played by William H. Macy runs out and drives away when being questioned by the lead detective, played by Frances McDormand. Her wonderful line was “Geez, the suspect’s fleeing the interview.” Mark’s results beautifully demonstrate that these T cells are, like that fleeing character in the movie, exquisitely sensitive to the inputs they are confronting. A second finding Mark described is that fugetaxis can be faster, as velocity, than chemotaxis, a profoundly interesting result. From here, Mark went on to describe the role of the chemokine CXCL12 in this regulated pathway, including studies with pancreatic islets. The concept here is how an immunologically privileged zone may be established with a chemorepellent agent and whether a chemokine like CXCL12 is a pro-survival factor (and thus allows these cells to live long enough to respond to new differentiation signals) or that it plays a more direct role. Mark also went on to describes contrary setting in ovarian cancer in which this mechanism is applied and can be antagonized to the advantage of the host. Mark showed how ovarian cancer over-expresses both CXCL12 and its cognate receptor, CXCR4 and thereby engineers a pro-survival and immune isolated environment for itself.