Lack of ACTH oversecretion from SCT has been related to two mechanism: The presence of a higher amount of lysosomes in the tumor’s cytoplasm, which causes premature destruction of ACTH before release (72); and disruption of POMC-product processing due to dysfunction or reduced expression of prohormone convertase 1/3 (PC1/3) resulting in an inability to synthesize mature ACTH molecules (Figure 1) (72, 73). The gene discussed is PCSK1; the disease is neoplasm.