In fact, a peculiar molecular mechanism operating during NSCLC progression upregulates TGF-betaR3 expression: this mechanism is driven by overexpression of HMGA2, a non-histone chromosomal high-mobility group protein; the high expression of HMGA2 mRNA determines a marked binding of let-7 family micro-RNA; this blocking of let-7 micro-RNA determines a derepression of typical let-7 targets and particularly of TGF-betaR3, that, through this mechanism, is derepressed and overexpressed and TGF-beta signaling is greatly potentiated in NSCLC [192]. Here, HMGA2 is linked to non-small cell lung carcinoma.