In prostate cancer models of acquired resistance to AR-targeted therapies, a critical role for JAK/STAT signaling has been identified in promoting an inflamed, stem-like precursor to NEPC.63,65 This same stem-like intermediate has been observed in other studies where in vivo systems were used to chart the transformation of normal luminal and/or basal precursor cell types into NE tumor types.68,156 However, it remains unclear when and how an inflamed or stem-like state may help evade key immune checkpoints in tumor control, leaving this as an area of active investigation. Here, SOAT1 is linked to neoplasm.