In another ovarian model, Xia et al. found that the immunosuppressive function of Tim4+ TAMs was mainly mediated by autophagy and the FAK family-interacting protein of 200 kDa (FIP200); further, they found that a deficiency in FIP200 could both result in Tim4+ TAMs’ death in the TME and promote T-cell-mediated anti-tumor immune response via the upregulation of ROS [155]. The gene discussed is RB1CC1; the disease is neoplasm.