By utilizing different exon–exon junction-spanning primer pairs (Figure 2A), we investigated APOL1 splice variation, both basally and upon IFN-γ induction, in two cellular systems: a human renal cell carcinoma (RCC) cell line, as a surrogate of the kidney, the primary site of APOL1’s cellular toxicity, and a hepatocellular carcinoma (HepG2) cell line, representative of the liver, the principal producer of serum APOL1 [73]. The gene discussed is APOL1; the disease is renal cell carcinoma.