In general, ILC2s isolated from lungs phenotypically have a higher number of ST2 receptors (35, 46–48) than ILC2s isolated from other organs, and, therefore, are able to respond rapidly to IL-33 stimulation, more significantly activating downstream signaling through ST2 receptors with consequent enhancement of cytokine-effector functions attracting more immune cells to the tumor site. Here, IL33 is linked to neoplasm.