Since our previous studies clearly showed that both genetic and pharmacological inhibition of Sphk1 prevented the development of hypertension-induced left ventricular cardiac hypertrophy, the primary aim of our study was to investigate the molecular effects of Sphk1 silencing in AngII-induced hypertrophy in vitro; however the usage of a neonatal CMs model allowed us to additionally recognize a heretofore unknown role of Sphk1 in neonatal CM development. Here, SPHK1 is linked to hypertensive disorder.