Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice. Overall design: Three control mice (Tmem1002loxP/2loxP) and three mutant mice (Tmem1002loxP/2loxP;ROSA26+/CreER) were treated with tamoxifen (two consecutive intraperitoneal injections, 0.1 mg/g of body weight) to activate CreER recombinase. Total RNAs were isolated from lungs 7 days after tamoxifen injection.