Given that ICIs activate T cells, which, in turn, stimulate osteoclasts by increasing RANKL and cytokine levels, the risk of osteoporosis and fractures associated with ICIs is considered to occur uniformly, regardless of the target of action of the ICIs (i.e., PD-1, PD-L1, or CTLA-4). This evidence concerns the gene TNFSF11 and osteoporosis.