As research has shown that IAPs can cause resistance to apoptosis and that the dys-regulation of IAPs can increase the threshold for apoptosis in cancer and lead to disease progression, we made the following hypothesis:

1. Insensitivity towards cancer treatment causing drug-induced apoptosis may be due to the over-expression of IAPs in breast cancerous cells. 

This led to us formulate our second hypothesis which complements the first: 

2. The inhibition of IAPs can lead to increase in apoptosis rate and overcome the intrinsic resistance of mus musculus mammary gland cells to targeted therapies against EGFR receptors, thereby increasing their efficiency.