Pim-1 differs from many other kinases in that it requires no post-transcriptional modification to become active, and therefore its activity is determined by its levels in the cell (21). Expressed at varying levels in most tissues, Pim-1 can be induced by cytokine stimulation, oxidative stress, and nutrient deficiency and can be thought of as an adaptive response to hostile surroundings. In this regard, Pim-1 is an interesting if not ideal choice as special equipment for cells that need to survive as long as possible in a foreign environment, without a blood supply or native matrix attachments. Cancer cells are expert at this type of survival, and indeed Pim-1 is a proto-oncogene, shown to be a weak tumor promoter when overexpressed alone and a strong tumor promoter in the presence of c-Myc gain of function ((22),23). By permitting cells to override normal blocks to mis-timed cell cycling, Pim-1 may enhance genome instability as part of its tumorigenic potential. A further concern is the fact that, in clinical practice, most autologous CPCs will be taken from older individuals with higher numbers of acquired somatic mutations and cancer risk. These issues will need to be addressed in future work. In the present study (14), although Pim-1–engineered cells persisted significantly longer after injection into the myocardium, they nonetheless were undetectable after 8 weeks, reducing concerns about their tumorigenic potential.