Indeed, taking advantage of the MKK7 and JNK1 fusion plasmid (MKK7-JNK1) engineered into a lenti-virus vector, which may activate JNK activity [39], we observed that artificial JNK activation rendered chemosensitive cancer cells K562 tolerant to Dox (Figure 6E), simultaneously increasing the Gli activity as reflected by QT-PCR analysis of the Gli1 expression (Figure 6F); while the negative control MKK7-JNK1(APF) for MKK7-JNK1 did not impact either the sensitivity of K562 cells to Dox (Figure 6E) or the expression of Gli1 at mRNA level (Figure 6F). This evidence concerns the gene GLI1 and cancer.