The dual role of Dectin-1 in tumor biology may be attributed to several factors: (1) Different tumors have distinct microenvironments that can shape Dectin-1’s function; (2) various immune cells express Dectin-1, and its activation in different immune cell types can lead to diverse functional outcomes; (3) and interactions between Dectin-1 and other membrane molecules can modulate their functions, further influencing tumor progression. This evidence concerns the gene CLEC7A and neoplasm.