ERBB2 and endometrial cancer: Consistent with these clinical data, we recently demonstrated that PIK3CA inhibitors (copanlisib and taselisib) and pan-c-erb-inhibitors (afatinib and neratinib), when used as single agents, while initially highly active in vivo against biologically aggressive endometrial cancer models, may rapidly induce the development of compensatory mechanisms of resistance including upregulation of phosphorylated (p)HER2/neu and pEGFR in PIK3CAi-treated/resistant tumors or upregulation of pAKT in neratinib-treated/resistant tumors (Lopez et al., 2014, Lopez et al., 2015).