Together, ATMs respond to their environment by upregulating lipid/lysosomal programs, which is likely heighted during obesity, allowing them to fulfill their main function of clearing up dying adipocytes, buffering lipids, preventing ectopic lipid spill over, and ensuing insulin resistance (25, 26, 33, 34). The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.