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The systemic and resistant nature of metastatic castration-resistant prostate cancers (mCRPC) renders them largely incurable even after intensive multimodal therapy. The proliferation, survival, metastasis, and epithelial-mesenchymal transition (EMT) are four vital events that are deeply linked to carcinogenesis. Hence, it is necessary to find a new combination of several therapies, targeting those vital mechanisms with minimal side effects. Significant research works have shown differential low expression of the metabolic Farnesoid X receptor (FXR) in primary and metastatic prostate cancer suggesting their importance in prostate cancer pathogenesis. Moreover, a fasting-mimicking diet (FMD) was introduced recently to reverse the metabolic reprogramming of cancer cells and promote cancer regression. Therefore, we hypothesized that FXR activation and FMD may inhibit proliferation and the metastatic phenotype in the androgen-independent prostate cancer cells.