Through this interaction, they promote the expansion of B-ALL cells by enhancing cellular proliferation and migration, likely via activation of pathways such as MAPK/ERK and downregulation of adhesion-regulating genes, while concurrently modifying the tumor microenvironment to suppress immune surveillance mechanisms through the induction of immune checkpoint molecules like PD-L1 or the downregulation of MHC class II expression in antigen-presenting cells [110,111]. Here, CD274 is linked to neoplasm.