The molecular mechanism at the basis of endothelial dysfunction, EndMT, fibrosis, and transition towards PH would involve the release of cytokines and the activation of signaling pathways related to protein kinase B (Akt), phosfoinositide-3-kinase (PI3K), and mitogen-activated protein kinases (MEK1/2), like extracellular signal-regulated-kinase1/2 (ERK1/2) and adenosine 5′-monophosphate activated protein kinase (AMPK) [15,16,17]. The gene discussed is AKT1; the disease is endothelial dysfunction.