We surmise that when anti-cancer treatments, such as anti-PD1/L1 and TKI, target cancer and CSC but may also damage the embryo and normal SC (e.g., MSC express PDL1, morphogenetic pathways involve tyrosine kinases), they may pose more risk to the fetus than pure immune modulatory agents (such as anti-CTLA4, IFN-alpha, IL-2) do, because the latter do not cause harm to normal SC and are less likely or unlikely to inflict injury to the developing fetus. The gene discussed is CTLA4; the disease is cancer.