AMPK and ULK1 were found to have a similar cytoprotective mechanism against chemotherapeutics in primary pancreatic cancer cells as well as pancreatic cell lines.192 Further, in a t(8;21) AML model, Kasumi‐1 cells survived short‐term treatment with histone deacetylase inhibitors by upregulation of autophagy.193 However, interactions between AMPK and mTOR were not investigated and long‐term resistance was not examined. The gene discussed is MTOR; the disease is acute myeloid leukemia.