We acknowledge several limitations. First, the experiment was performed using a human osteosarcoma cell line (MG63), whereas the use of a primary human osteoblast cell culture might better replicate what happens in humans in vivo. We chose the MG63 cell line because these cells show a phenotype similar to that of normal human osteoblasts, while also providing a reproducible experimental model suitable for the microarray analysis. Second, as it is still difficult to explain the roles of all genes, whose expression was modified, we focused on the role of genes with well-known functions related to osteogenesis. Third, although microarray technology is widely accepted as a valid approach to describe changes induced by a factor on cell environment, additional research using, for example RT-PCR, might be useful to provide supplementary support for the results obtained. Fourth, we studied responses at only one time. We chose 18 hours exposure time on the basis of a previous time experiment, in which a peak in DNA synthesis was seen after 18 hours of stimulation in MG63 cultures maintained in the presence of 10% FCS [45] . In contrast, Lohmann et al. reported PEMFs enhanced cell differentiation in MG63 cultures and reduced cell proliferation [30] . The differences existing between the two sets of data regarding cell proliferation could be related to the different experimental conditions used. Lohmann et al. exposed MG63 cultures when they reached confluence. When cultures are confluent they stop to proliferate. We exposed cells to PEMF when cultures were subconfluent, therefore, they responded with an enhancement of proliferation. We cannot extrapolate our findings to shorter or longer exposures to PEMFs. PEMFs appear to act on bone formation by inducing upregulation of several genes related to osteoblast proliferation and differentiation. Among those genes, HOXA10, a transcriptional factor that acts positively on RUNX2, is the main transcriptional regulator of osteoblast differentiation [25] . HOXA10 controls osteoblastogenesis via RUNX2-promoted osteoprogenitor cell differentiation in immature osteoblasts [25] . This protein also is believed to be involved in activation of alkaline phosphatase, osteocalcin, and sialoprotein genes [25] . We also observed * SAM assigns a score to each gene on the basis of a change in gene expression relative to the standard deviation of repeated measurements. STAT3, P2RX7, and AKT1 upregulation. It has been suggested that osteoblast-specific disruption of STAT3 results in an osteopenic phenotype [27, 41] . STAT3, involved in bone turnover [27] , regulates the transcription of various genes that modulate cell proliferation and differentiation in a cell-specific manner [27] . P2RX7 is a purinergic receptor, which is correlated with calcium channels and interacts with the calmodulin-dependent protein [37] . Activation of P2RX7 receptors by exogenous nucleotides stimulates expression of osteoblast markers and enhances mineralization in cultures of rat calvarial cells promoting osteogenesis [37] . V-akt murine thymoma viral oncogene homolog 1 (AKT1), is a phosphoinositidedependent serine-threonine protein kinase, and one of the key players in the signaling of potent bone anabolic factors [29] . The disruption of AKT1 in mice led to low-turnover osteopenia through dysfunction [29] . AKT1 deficiency causes decreased bone mass and formation [29] , impairs RUNX2-dependent differentiation and function of osteoblasts [29] , and impairs bone resorption via dysfunction of osteoblasts and osteoclasts [29] . AKT1 suppresses osteoblasts apoptosis through inhibition of FOXO3a and Bim [29] , and may mediate the osteoblastic bone formation by IGF-1 [29] . The IGF-1/AKT1 pathway might be a common pathway for bone anabolic action of parathyroid, thyroid, and growth hormone [29] . We also observed upregulation of genes involved in connective and bone tissue formation (COL1A2) and noncollagenous extracellular matrix (ECM) synthesis (SPARC, FN1, VCL). COL1A2 encodes for collagen Type 1a2. Collagen Type 1 is the most represented collagen in the human organism and is important for ECM stability [6] . Osteonectin (SPARC), the most abundant noncollagenous protein in bone tissue, modulates cell-matrix interaction and is involved in the tissue-remodeling process [47] . FN1 is important for ECM stability and involved in adhesion and migration cellular processes such as tissue healing [39] . VCL is a cytoskeletal protein associated with the intercellular junctions between the cells and the matrix [49] .