To confirm their interactions, we first treated tumor cells with actinomycin D to assess the rate of TP53INP1 mRNA decay and found that the half-life of TP53INP1 mRNA was significantly extended in MSI2a-overexpressing TNBC cells (Fig. 6b) but significantly shortened in MSI2a-knockdown TNBC cells (Fig. 6c). The gene discussed is TP53INP1; the disease is neoplasm.