Major implication of the Gli-1

I.  The Gli-1 gene
affects the following other genes
---PDGFR in mesenchymal tissue
---FOXM1
---Sufu
---SP1, USF1
---Twist1
---CyclinD2
---Plakoglobulin
---Shh

II. PTCH1:  Act as a receptor to the Hedgehog ---the contact releases the SMO
Revant Info-Vismodegib
"The substance acts as a cyclopamine-competitive antagonist of the smoothened receptor (SMO) which is part of the hedgehog signaling pathway.^[2] SMO inhibition causes the transcription factors GLI1 and GLI2 to remain inactive, which prevents the expression of tumor mediating genes within the hedgehog pathway.^[4] This pathway is pathogenetically relevant in more than 90% of basal-cell carcinomas.<sup>[5]"wikipedia

link to chondrosarcoma is most puzzling
role in bladder cancer still to be explored, mostly I guess in the squamous type?
in Medulloblastoma?</sup>

Example of neoplastic phenomena at work.

One example  of constant  stimulation is an estrogenic supply which leads to type I endometrial cancers. It appears that constantly giving Estrogens unopposed by progestins  leads to the stimulation of many genes including Grb2, a" wild gene" that provokes amplification of critical genes that are controlling the epithelium of the Uterus (Catenins and Muc1) leading to the disturbance of cell polarity and adhesions, events that are preceding hypertrophic transformation.  MUC 1 amplification will shield the cell from immune detection.  How much Sp1, EP 300, and RELA play to further broaden NF-kB amplification in this process remains to be further defined.
RELA is another "wild gene" very much in control of epigenetic phenomena induced by amplification of the NF-kB.
"RELA has been shown to interact with:

• APBA2,^[3]
• AHR,^[4][5]
• ASCC3,^[6]
• BRCA1,^[7]
• BTRC,^[8]
• C-Fos,^[9]
• C-jun,^[9]
• C22orf25,^[10]
• CSNK2A1,^[11]
• CDK9,^[12]
• CEBPB,^[13][14]
• CREBBP,^{[15][16][17][18][19]}
• CSNK2A2,^[11]
• DHX9,^[20]
• EP300,^[19][21]
• ETHE1,^[22]
• FUS,^[23]
• HDAC1,^[16][21][24]
• HDAC2,^[21][25]
• HDAC3,^[26]
• ING4,^[27]
• IκBα,^{[8][21][26][28][29][30][31]}
• MEN1,^[32]
• MTPN,^[33]
• NCF1,^[34]
• NFKB1,^[35][36]
• NFKB2,^[35][37]
• NFKBIB,^[38][39]
• NFKBIE,^[40]
• NR3C1,^[41][42][43]
• NCOR2,^[44][45]
• PARP1,^[46]
• PIAS3,^[15]
• POU2F1,^[47]
• PPP1R13L,^[48][49]
• PRKCZ,^[50]
• REL,^[29][35][51]
• RFC1,^[52]
• RNF25,^[53]
• SP1,^[54][55]
• STAT3,^[56][57]
• TAF4B,^[58]
• TBP,^[59][60]
• TP53,^[57] and
• TRIB3.^{[61]" (wikipedia}
• 
  
• ^{note the NR3c1 (Androgen) where progestins intervene to amend estrogenic effects potentially!}