This is reflected in mice models, where systemic Sdhb heterozygosity is insufficient to induce tumour formation [10,11], Sdhb knock-out in medullary adrenal cells solely led to increased succinate levels in the absence of other PPGL hallmarks, but additional Nf1 mutations induced SDHx-like PPGLs [30]. The gene discussed is SDHB; the disease is neoplasm.