The observed Glycoside-O-4 expression changes are specific to this inducer of hypertrophy. Further studies will be required to test the impact of other well-established prohypertrophic agents. When using an in vitro system for disease modeling in humans it is critical to characterize and validate it to confirm it��s efficiency. To achieve this for our cardiac hypertrophy model, we first performed RT-qPCR on several classical hypertrophy markers to detect any changes in their expression levels between the controlCMs and ET1-CMs. We observed significant expression changes treatment of heart failure and LVH. We identified the genes that were loaded in PC2 and also show significant differential expression in our model. A gene set enrichment analysis was then performed on the overlapping genes to identify the major disease phenotypes associated with these genes. From this analysis, we detected stress, cardiovascular disease and hypertrophy to be some of the significantly enriched diseases. These results provide strong evidence that the observed in vitro changes induced by ET-1 recapture a specific subset of expression changes observed in vivo in humans with LVH. This approach of comparing the relevant phenotype in the originating disease tissue and the hypertrophic hiPSC-CM provides a novel methodology for validation of disease models. There has been increasing evidence on the role played by miRNAs in the regulation of cardiovascular development and disease mechanisms. A cardiac hypertrophy model based on ECG iPSCderived cardiomyocytes provides a unique system to study miRNA expression changes associated with the disease phenotype. To interrogate the hypertrophy driven miRNA expression differences in our hiPSC-CMs, we performed miRNA-Seq and expression analysis. We detected more than 250 known human mature miRNAs with significant differential expression between ET1CMs and control-CMs. These include known miRNAs both associated with and those not previously linked to cardiac hypertrophy. Of the previously established hypertrophy miRNAs, we found hsa-miR-23a-3p, hsa-miR-22-3p and hsa-miR-208a-3p to have significant differential expression.