In BC, the hormonal status (Estrogen Receptor (ER)-positive and ER-negative) affects how IGF1-Ea and IGF1-Ec influence cell proliferation, progression, and resistance to therapy through interaction with ER, particularly in ER-positive cases [75,76] The absence of IGF1-Eb transcripts may enhance cancer cell aggressiveness, while studies debate its role as an anti-cancer factor by inhibiting BC cell growth, invasion, and angiogenesis [75], while in CC, human papillomaviruses (HPVs) interact with IGF axis components, potentially influencing spliceosome elements [74]. This evidence concerns the gene ESR1 and cancer.