Consistent with Xiang et al. results, SR18292 led to oxidative damage and energy exhaustion, significantly inhibited the proliferation of multiple myeloma cells, and inhibited tumor growth in myeloma model mice.70 Similarly, in cholangiocarcinoma, SR18292 also reduced PGC1α levels, mitochondrial mass, and mice with tumor xenografts growth.71 Collectively, these data indicated that SR18292 induced an energy crisis, which can be employed as a pharmacological target for cancer treatment. This evidence concerns the gene PPARGC1A and AL amyloidosis.