Transcriptional analysis supported the predominant obesity‐induced myocardial maladaptation, which generally occurs in the presence of reinitiated foetal gene expression and elevated Ca2+‐induced transcription.17, 25 In that regard, a clear obesity‐driven switch from MYH6 to MYH7 was noticed, as well as elevated transcription of RCAN1, a defined target gene of the Ca2+‐responsive transcription factor NFAT.26 The RNAseq data also underscored the notion that diastolic dysfunction‐associated hypertrophy can develop in absence of a severe increase in cardiac afterload. The gene discussed is MYH6; the disease is obesity disorder.