In brief, recalling what has been documented for the viral counterpart, vaccinal Spike has the potential to (i) deplete membrane-bound and soluble ACE2 (see Section 5.1); (ii) trigger the oncogenic ERK/MAPK, EGFR-AKT, AXL, and SNAIL-TGFβ pathways (see Section 5.1 and Section 5.2); (iii) interact with ERs in breast cancer cells (see Section 5.2), (iv) interfere with tumor suppressor TP53 stability and transcriptional activity (see Section 5.3); (v) induce the formation of syncytia (see Section 5.4). The gene discussed is SNAI1; the disease is breast cancer.