MARCKSL1 and neoplasm: Since F‐actin‐rich membrane structures at the leading edge of migrating cells could form invadopodia that engage in proteolytic activity and degrade the surrounding extracellular matrix (ECM) to facilitate tumor cell penetration through the epithelial and endothelial basement membranse and because there is colocalization between MARCKSL1 and F‐actin at the leading edge of the cell, we speculate that MARCKSL1 participates in the formation of invadopodia to modulate cell mobility.