Thalidomide was developed in the 1950s as a sedative drug and withdrawn in 1961 
because of its teratogenic effects, but has been rediscovered as an 
immuno-modulatory drug. It has been administered successfully for the treatment 
of erythema nodosum leprosum, aphthous ulceration and cachexia in HIV disease, 
inflammatory bowel diseases, and several malignant diseases. The suppressive 
effect of thalidomide on the activation of the nuclear transcription factor 
NF-κB may explain these effects of thalidomide. NF-κB is retained in the 
cytoplasm with IκBα, and is activated by a wide variety of inflammatory stimuli 
including TNF, IL-1 and endotoxin followed by its translocation to the nucleus. 
Angiogenesis and organogenesis also require gene transcription and signal 
translocation. The findings shed new light on the anti-inflammatory properties 
of thalidomide and suggest pharmaceutical actions of thalidomide via 
interference of transcription mechanism. I reviewed the effects of thalidomide 
on auto-inflammatory diseases of childhood.