While the aforementioned PS-out approach using either a CDC50 flippase engineered cell or the ATP11B negative cells provides an important conceptual rationale for the PS exposure on tumor cells as a cell intrinsic mechanism that drives immune escape, an equally important aspect of dysregulated PS in the tumor microenvironment that still requires better understanding is how tumor cells, versus tumor associated stroma cells, vascular cells, or immune cells (or both) contribute to the totality of constitutive PS externalization in solid tumors. The gene discussed is ATP11B; the disease is neoplasm.