DO NOT UNDERESTIMATE THE POWER OF ONE (RECEPTOR)

"IRAK1b, a Novel Alternative Splice Variant of Interleukin-1 Receptor-associated Kinase (IRAK), Mediates Interleukin-1 Signaling and Has Prolonged Stability*"

Liselotte E. Jensen‡"

Please just go to article, but it is clear that TGF Beta is clearly important particularly in Breast Cancer.  Anything that can autophosphorylate should make any-researcher nervous because it can set its self up and initiate something up (driver mutation).  When it is a molecule that can help cancer cell elude autoimmune destruction, when it help the auto-growth, and avoid apoptosis through death receptor or otherwise, when it interfere with cellular differentiation, when its level is require at strong presence, and when it is a conserved mechanism, it is an important part of the neoplastic transformation.   Through the Tollip, it can be reached by targeting the Tankyrase!  CRBCM is on it!
IRAK-1 is a critical component to cancer production!
Involvement of the NFKB suggests it (through TRAF 6, PKC, and TAB)
Through the RACs and RICs, IRAK reaches Metastasis (Rho/ROCK) and the BARC1 (breast cancers). (by touching Myd...of course).
Its activity through tampering with a gene regulator (IKK) should make you double nervous and doubling with autophosphorylation means it can be a driver on its own and achieve autocrine role for the new Cancer!

Through the CHUK it acts as a multiple site hitting of the NFkB but also reaches the Wnt through CTNNB1. Hitting NCOA means the engagement of all other Hormone receptors including the "wild" gene, Andogene receptors!  Once again The Tankyrases better be your Target to stop all this upstream...
And you know through the Dead Box, P53 will be spared and through mechanisms shared above, your Retinoblastoma gene will soon come into play.  And I guess I should not mention the Ubiquitin C or the NOTCH!...they all are involved!

The lesson here is that it is not the gene to look at when you are trying to find a therapeutic intervention, it is its common Receptor or substrate.  Don't look at IL-1, look at their receptors ...such as IRAK-1!