Mutations in the human <i>MYH7</i> gene, encoding a slow skeletal muscle/-cardiac myosin heavy chain, cause different types of myopathies. The nematode model <i>Caenorhabditis elegans</i> has frequently been employed to study the molecular and physiological consequences of <i>MYH7</i> mutations in muscle function by introducing mutations into the <i>
unc-54</i> gene, the worm <i>MYH7</i> ortholog. We report here that the <i>C. elegans</i> model is not appropriate for such studies if they involve expression of the UNC-54 protein (wild-type or fused to green fluorescent protein) above endogenous levels.