Emerging therapies for HF aim to normalize dysregulated Ca2+ handling by inhibiting CaMKII hyperactivity (using peptides like AIP, KN 93, or new small-molecule inhibitors [9]), stabilizing leaky ryanodine receptor type 2 (RyR2) channels (Rycals such as ARM210 to prevent diastolic Ca2+ leak [10]), and selectively modulating L-type Ca2+ currents (e.g., enhancing Rad–LTCC inhibitory interactions or blocking re-expressed Cav1.3 channels [11]). Here, CACNA1D is linked to hydrops fetalis.