Considering that SMARCA4 is an epigenetic factor and BLVRA was shown to interact directly with MEK/ERK and serve as an ERK activator (Lerner‐Marmarosh et al., 2008), we speculate that SMARCA4 might function downstream of BLVRA/MEK/ERK, which is in line with our finding that overexpression of the Drosophila BLVRA homologue dBVR alone led to dopaminergic degeneration and aggravated degenerative phenotypes in multiple PD models, which could be remarkably rescued by inactivation of the Drosophila homologue of SMARCA4 (Brm). This evidence concerns the gene MAP2K7 and Parkinson disease.