AKT1 and breast cancer: Conversely, TNFR2-activated PI3K/Akt and phosphoinositide 3-kinases (PI3K)-protein kinase B/serine-threonine kinase (PKB/Akt) can mediate BC cell survival by inducing cellular growth factors, such as insulin-like growth factor 1 (IGF-1), promoting drug resistance, and preventing of DNA damage in cancerous cells [42–46].