It is hypothesized that expression of β-slow MyHC in the absence of CLFS in denervated fast muscle and in hypothyroidism is due to the reversion to the mechanism of β-slow MyHC expression of slow primary myotubes sustained by Sox6/MEF-2C pathway (Taglietti et al. 2016), in common with soleus fibres of slow primary ontotype. The gene discussed is MYH6; the disease is hypothyroidism.