Treatment of lung epithelial cells with different kinds of nanosized particles leads to cell proliferation. As bigger particles fail to induce this reaction, it is suggested that the special surface properties, due to the extremely small size of these kind of materials, is the common principle responsible for this specific cell reaction. Here, the activation of the protein kinase B (AKT) signaling cascade by carbon nanoparticles was investigated with regard to its relevance for proliferation. Kinetics and dose response experiments demonstrated that AKT is specifically activated by ultrafine carbon particles in rat alveolar type II epithelial cells as well as in human bronchial epithelial cells. This pathway appeared to be dependent on EGF-R and 1-integrins. The activation of AKT by these receptors is known to be a feature of adhesion-dependent signaling. However, intracellular proteins described in this context (pp125^FAK and ILK) were not activated, indicating a specific signaling mechanism. Inhibitor studies demonstrate that nanoparticle-induced proliferation is mediated by PI3-kinase and AKT. Moreover, overexpression of mutant AKT, as well as pre-treatment with the AKT inhibitor SH-5, reduced nanoparticle specific ERK1/2 phosphorylation which is decisive for nanoparticle-induced proliferation. With this report, we describe the activation of a pathway by carbon nanoparticles which was so far known to be triggered by ligand receptor binding or upon cell adhesion to extracellular matrix proteins.