Dysregulation of cell stemness phenotype (e.g., β‐catenin and CD133), cell–cell interaction (e.g., CD44 and E‐cadherin), and cell–matrix interaction (e.g., matrix metalloproteinase) as well as of inflammation (e.g., cytotoxic T cells) are essentially involved in tumor budding [53]. Here, PROM1 is linked to neoplasm.