Infantile hemangiomas (IHs) are the most common benign tumors in early childhood. They show a distinctive mechanism of tumor growth in which a rapid proliferative phase is followed by a regression phase (involution). Propranolol is an approved treatment of IHs, but its mechanism of action remains unclear. We integrated and harmonized data from three sources: a) high-throughput genomics data on IHs, b) toxicogenomics data from propranolol exposure, and c) microRNA data from IHs and propranolol exposure. Our integrative data approach lead to subsets of putative biomarkers for proliferation and involution. We revisited propranolol mechanism of action based on toxicogenomics putative biomarkers, namely EPAS1, LASP1, SLC25A23, MYO1B, and ALDH1A1 that recapitulate some of the pathways by which propranolol expedite the involution phase of IHs.