More interestingly, after validation by real-time RT-qPCR in a larger group of patients, a human panel of adult and fetal tissue samples, the authors confirmed the loss of circRNA formation from host genes CAMK2D (in DCM and HCM) and titin (mainly in DCM) in disease, and disease-regulated changes in circRNA production are independent of transcriptional regulation. The gene discussed is CAMK2D; the disease is familial dilated cardiomyopathy.