In contrast, moderate cardiomyocyte KD (using GMH5) of pax, talin, pinch, as well as mys, exhibited a low AI, typical of 1-week control heart and importantly failed to show any significant age-dependent elevation of AI, unlike their wild-type controls (Fig. 6), thus strongly suggesting a similar beneficial effect of fine-tuned reduction in gene function as with ilk or mys. Interestingly, weak talin KD did not show increased arrhythmias at young ages, but already resulted in some disorganization in myofibrillar structure (Fig. S4I,J). This evidence concerns the gene LIMS1 and cardiac arrhythmia.