We find that that combining strategies to 1) modulate cytotoxic macrophage composition in the tumor microenvironment (e.g., CSF1R inhibition), 2) enhance macrophage targeting (e.g., antibody or CAR-based approaches), and 3) impair tumor membrane repair (e.g., ATG9A depletion) together can achieve complete tumor responses independent of T-cells. Here, CSF1R is linked to neoplasm.