In this field, different strategies include the blockade of monocyte recruitment, TAM depletion, TAM reprogramming into the immunostimulatory M1 subtype, molecular signaling modifications (such as the inhibition of immunosuppressive molecules produced by TAM and CD47/SIRPα checkpoint) and the reversal of drug resistance by targeting the cross-talk between TAM and tumor cells [129,130,131,132,133,134,135,136,137,138,139,140,141,142,143,144,145,146,147,148,149,150]. Here, SIRPA is linked to neoplasm.