Under low sterol conditions, which disrupt the Insig‐SCAP interaction, COPII mediates SCAP‐SREBP complex transport from the ER to the Golgi apparatus,[4, 11] where the SREBPs are cleaved by the S1P and S2P proteases to yield active amino‐terminal fragments that enter the nucleus for gene transcription.[1, 12] The subsequently increased sterol content restores the Insig‐SCAP interaction, thereby inhibiting SREBP activation and forming a feedback loop.[3, 13, 14] However, in tumor cells, oncogenic signaling activates SREBP independent of the intracellular sterol level. The gene discussed is SCAP; the disease is neoplasm.