Homeostasis of platelet number in human and other mammals is well maintained for prevention of minor bleeding and for other im-munological functions, but the exact molecular mechanism responsible for immune thrombocytopenic purpura (ITP) has not been fullyunderstood. In an effort to identify genetic factors involved in initiation of platelet production in response to bleeding injury or plateletdestruction, we have successfully generated an animal model of human ITP via intraperitoneal injection of anti-platelet antibody into theBalb/c mouse. Platelet counts were dropped dramatically in animals that received antibody injection within 4 h, maintained at the mini-mum level for a period of 44 h, started to rebound after 48 h, and reached to the maximum at 144 h (6 days). Final homeostasis reached atapproximately 408 h (17 days), following a minor cycle of platelet number fluctuation. Using semi-quantitative RT-PCR, we assessed andcompared mRNA level of CD41, c-myb, c-mpl, caspase-3, caspase-9, GATA-1, and Bcl-xl in bone marrow and spleen. Alteration ofmRNA expression was correlated with the change of platelet level, and an inverse relationship was found for expression of the genes be-tween bone marrow and spleen. No transcription was detectable for any of the seven genes in bone marrow at the time when plateletnumber reached the maximum (144 h). In contrast, mRNA transcripts of the seven genes were found to be at the highest level in spleentissue. This is the first study of simultaneous detection of multiple platelet related genes in a highly reproducible ITP animal model. Ourresults provided the supportive evidence that expression of the above seven genes are more related to negative regulation of plateletnumber in spleen tissue, at least in the model animals.