In the present study, (1) we investigate how the different expression levels of the targeted receptor PSMA on prostate cancers may affect the microdistributions of the PSMA‐targeting antibody and, therefore, the best radioactivity split ratio(s) for inhibiting cancer cell growth in the presence of transport barriers, and (2) we systematically interrogate the effect of different radioactivity split ratios between the two carriers (tumor‐responsive liposomes and the PSMA‐targeting antibody) on inhibiting the growth of PSMA‐expressing prostate cancers in vivo. The gene discussed is FOLH1; the disease is neoplasm.