This conversion is achieved by an unconventional set of steps, including the activation of pro-tumorigenic signaling in osteoclasts and the enrichment of atypical tumor-suppressing proteins such as Hsp90ab1, Eno1, and Ubc in the secretome, followed by the interactions of Hsp90ab1 and Eno1 with a moonlighting protein, CD44. The gene discussed is ENO1; the disease is neoplasm.