Notably, the presence of an active mTOR Complex1 (mTORC1) in DCM samples could account for many of the above reported alterations, since it suppresses lysosomal biogenesis, promoting the exclusion of TFEB from the nucleus [23], and inhibits autophagy, promoting both ULK1 phosphorylation [37] and inhibition of TFEB-dependent transcription of autophagy genes [38,39]. The gene discussed is ULK1; the disease is familial dilated cardiomyopathy.