C1 referred to the low stemness subtype with the improved clinical outcomes, displayed predominant mutations in multiple oncogenes and tumor suppressors, such as TP53, SYNE1, MUC16, and PIK3CA. The high mutational load tends to produce more neoantigens, which could further induce the proliferation and activation of T cell to eliminate tumor cells (37). Here, SYNE1 is linked to neoplasm.