SH3GL1 and AL amyloidosis: In support to our "Geneticremittance" hypothesis, we predicted that if the M. tuberculosissRNA_1096 is present or predisposes to human, it may modulatehuman SH3GL1 (SH3-domain GRB2-like 1) which plays a role inendocytosis [71], regulation of cell cycle in leukaemia [72],positive regulation of cell proliferation and inhibition ofapoptosis in multiple myeloma [73], and oncogenesis in gliomas[74].