The overexpression of a PPGL-causing SDHB mutation or the knockdown of wild type SDHD protein (both resulted in the increased intracellular concentration of oncometabolite succinate) led to ACC proliferation and corresponding changes of the downstream genes including GIPC2, p27, p18, phosphor-pRb, and phospho-ERK, similar to the RET mutant (Fig. 6A, B). The gene discussed is RET; the disease is adrenal cortex carcinoma.