Previous studies revealed the synergistic effect of the SWI/SNF complex with other epigenetic factors, including histone acetylase and Rb1, on genome transcription (Strobeck et al., 2000; Chatterjee et al., 2018), while SMARCC1 functions as a scaffold structure in the SWI/SNF complex to undertake coordination with other epigenetic factors (Chatterjee et al., 2018), even though we observed a significant upregulation of β-catenin in the nuclear fraction of PCa cells with SMARCC1 depletion in our study, indicating that the PI3K/AKT pathway mediates the pro-oncogenic effects of SMARCC1 loss. This evidence concerns the gene AKT1 and posterior cortical atrophy.