Further, research has indicated that inflammation-induced apoptosis is modulated by interleukin-10 (IL-10), which can inhibit the apoptosis of VSMCs via the JAK2-STAT3 signaling pathway during atherosclerosis development.[94] Intrinsic apoptosis pathway may also play a role, as JAK2-STAT3 activation can enhance Bcl-2 expression and inhibit programmed cell death.[95]. The gene discussed is JAK2; the disease is atherosclerosis.