Moreover, overexpression of HSD3B7, or administration of the most abundant primary BA TCA, or treatment with the supernatants from AML12 after blocking endogenous miR-122, significantly promoted tumor cell growth (Figures 7C–7E and S6), whereas the DNA replication of cancer cells was diminished by the supernatants from cells overexpressing miR-122 or siHSD3B7 (Figure 7F). This evidence concerns the gene HSD3B7 and neoplasm.