Only one aforementioned in vitro study used a pro-apoptotic medicine, doxazosin, as the model of heart failure in a mouse atrial myocyte tumour cell line HL-1, and found that treatment with LCA reduces cell viability and that this effect was mediated by the decreased phosphorylation of EphA2 and the increased expression of total EphA2 in the doxazosin-induced apoptosis models of heart failure in HL-1 cells. Here, EPHA2 is linked to Leber congenital amaurosis.