Similarly to the rat failing cells, we found that, in human DCM cells, α1C-tubulin (TUBA1C), β2A-tubulin (TUBB2A), TUBB3, TUBG1, and MAP4 were significantly upregulated as compared to non-failing cardiomyocytes, suggesting a primary role for microtubule disruption in cellular vulnerability to MiCai generation (Figure 6E). This evidence concerns the gene TUBA1C and familial dilated cardiomyopathy.