Of note, treatment with the N-BP zoledronate, a drug commonly used for osteoporosis treatment that, in part, mediates its effects via the functional inhibition of the mevalonate pathway and small GTPases (Figure 3a), restored ERK5 activity in differentiated human MSC-derived osteoblasts, and re-induced PTHLH expression in those cells via an ERK5- and KLF2-dependent mechanism [73]. This evidence concerns the gene KLF2 and osteoporosis.