Significantly decreased receptor transcript levels in SSc lung fibroblasts with normal steady-state protein receptor levels could indicate high mRNA turnover, increased sensitivity to endogenous IGF-II expression, increased receptor protein half-life, altered nonsense-mediated decay, and/or decreased receptor degradation/turnover, thus affecting increased signal amplification downstream of the IGF-II: receptor interaction. The gene discussed is IGF2; the disease is systemic sclerosis.