Disruption of MAM‐mediated lipid transport constitutes another key mechanism, as demonstrated by mitotane, the only approved chemotherapeutic agent for the treatment of adrenocortical carcinoma (ACC) [248], which induces the accumulation of toxic lipids, including free and oxidized cholesterol, in ACC cells by inhibiting sterol O‐acyltransferase 1 (SOAT1), thereby triggering lipotoxic ERS [242]. The gene discussed is SOAT1; the disease is adrenal cortex carcinoma.