Similarly, CD26 drives keloid fibroblast proliferation and invasion through IGF-1/IGF-1R-mediated PI3K/Akt/mTOR activation, promoting mTOR downstream effectors (P70S6K, 4E-BP1); inhibition of CD26 or IGF-1R abrogates these effects, underscoring their central role in keloid progression (Guo et al., 2023; Wang and Liu, 2024; Xin et al., 2020). This evidence concerns the gene IGF1R and keloid.