The interaction between AKAP150 and long QT syndrome 8 (LQT8) is also known as Timothy syndrome and is characterized by a single amino acid substitution (G406R) in the L‐type Ca2+ (CaV1.2) channel.87 Disruption of AKAP150 improves pathological CaV1.2‐LQT8 channel gating and arrhythmias and prevents hypertrophy of LQT8 hearts by decreasing Ca2+ influx via CaV1.2‐LQT8 channels.88 The gene discussed is CACNA1C; the disease is long QT syndrome 8.